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Journal articles on the topic 'Disease programming'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

BARKER, D. J. P. "In utero programming of chronic disease." Clinical Science 95, no. 2 (August 1, 1998): 115–28. http://dx.doi.org/10.1042/cs0950115.

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1.Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. 2.These ‘programmed' changes may be the origins of a number of diseases in later life, including coronary heart disease and the related disorders stroke, diabetes and hypertension. 3.This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.

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2

김민형. "Fetal Programming and Adult Disease." JOURNAL OF THE KOREAN SOCIETY OF MATERNAL AND CHILD HEALTH 21, no. 1 (January 2017): 1–13. http://dx.doi.org/10.21896/jksmch.2017.21.1.1.

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3

Alexander, Barbara T. "Developmental Programming of Cardiovascular Disease." Colloquium Series on Integrated Systems Physiology: From Molecule to Function 5, no. 1 (June 27, 2013): 1–77. http://dx.doi.org/10.4199/c00084ed1v01y201305isp038.

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4

Falcão, Mário Cícero. "Fetal programming and future disease." Revista do Hospital das Clínicas 59, no. 6 (2004): 319–20. http://dx.doi.org/10.1590/s0041-87812004000600002.

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5

Bollinger, Lance M., Celsi E. Cowan, and Thomas P. LaFontaine. "Exercise Programming for Parkinsonʼs Disease." Strength and Conditioning Journal 34, no. 2 (April 2012): 55–59. http://dx.doi.org/10.1519/ssc.0b013e31824db335.

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6

Astorino, Todd A., and Matt M. Schubert. "Exercise Programming for Cardiovascular Disease." Strength and Conditioning Journal 34, no. 5 (October 2012): 60–64. http://dx.doi.org/10.1519/ssc.0b013e31825ab1aa.

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7

Vehaskari, V. Matti. "Prenatal programming of kidney disease." Current Opinion in Pediatrics 22, no. 2 (April 2010): 176–82. http://dx.doi.org/10.1097/mop.0b013e328336ebc9.

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8

Lau, C., J. M. Rogers, M. Desai, and M. G. Ross. "Fetal Programming of Adult Disease." Obstetric Anesthesia Digest 32, no. 2 (June 2012): 78–79. http://dx.doi.org/10.1097/01.aoa.0000414057.17428.db.

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9

Kratimenos, Panagiotis, and Anna A. Penn. "Placental programming of neuropsychiatric disease." Pediatric Research 86, no. 2 (April 19, 2019): 157–64. http://dx.doi.org/10.1038/s41390-019-0405-9.

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10

Thornburg, K. L. "The programming of cardiovascular disease." Journal of Developmental Origins of Health and Disease 6, no. 5 (July 15, 2015): 366–76. http://dx.doi.org/10.1017/s2040174415001300.

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In spite of improving life expectancy over the course of the previous century, the health of the U.S. population is now worsening. Recent increasing rates of type 2 diabetes, obesity and uncontrolled high blood pressure predict a growing incidence of cardiovascular disease and shortened average lifespan. The daily >$1billion current price tag for cardiovascular disease in the United States is expected to double within the next decade or two. Other countries are seeing similar trends. Current popular explanations for these trends are inadequate. Rather, increasingly poor diets in young people and in women during pregnancy are a likely cause of declining health in the U.S. population through a process known as programming. The fetal cardiovascular system is sensitive to poor maternal nutritional conditions during the periconceptional period, in the womb and in early postnatal life. Developmental plasticity accommodates changes in organ systems that lead to endothelial dysfunction, small coronary arteries, stiffer vascular tree, fewer nephrons, fewer cardiomyocytes, coagulopathies and atherogenic blood lipid profiles in fetuses born at the extremes of birthweight. Of equal importance are epigenetic modifications to genes driving important growth regulatory processes. Changes in microRNA, DNA methylation patterns and histone structure have all been implicated in the cardiovascular disease vulnerabilities that cross-generations. Recent experiments offer hope that detrimental epigenetic changes can be prevented or reversed. The large number of studies that provide the foundational concepts for the developmental origins of disease can be traced to the brilliant discoveries of David J.P. Barker.

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11

Barker, David J. P. "Intrauterine programming of adult disease." Molecular Medicine Today 1, no. 9 (December 1995): 418–23. http://dx.doi.org/10.1016/s1357-4310(95)90793-9.

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12

Buckley, Alex J., Anne L. Jaquiery, and Jane E. Harding. "Nutritional programming of adult disease." Cell and Tissue Research 322, no. 1 (April 22, 2005): 73–79. http://dx.doi.org/10.1007/s00441-005-1095-7.

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13

Moritz, Karen M., Wee Ming Boon, and E. Marelyn Wintour. "Glucocorticoid programming of adult disease." Cell and Tissue Research 322, no. 1 (April 22, 2005): 81–88. http://dx.doi.org/10.1007/s00441-005-1096-6.

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14

Lau, Christopher, John M. Rogers, Mina Desai, and Michael G. Ross. "Fetal Programming of Adult Disease." Obstetrics & Gynecology 117, no. 4 (April 2011): 978–85. http://dx.doi.org/10.1097/aog.0b013e318212140e.

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15

Hsu, Chien-Ning, and You-Lin Tain. "Developmental Origins of Kidney Disease: Why Oxidative Stress Matters?" Antioxidants 10, no. 1 (December 30, 2020): 33. http://dx.doi.org/10.3390/antiox10010033.

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The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.

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Hsu and Tain. "The Good, the Bad, and the Ugly of Pregnancy Nutrients and Developmental Programming of Adult Disease." Nutrients 11, no. 4 (April 20, 2019): 894. http://dx.doi.org/10.3390/nu11040894.

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Maternal nutrition plays a decisive role in developmental programming of many non-communicable diseases (NCDs). A variety of nutritional insults during gestation can cause programming and contribute to the development of adult-onset diseases. Nutritional interventions during pregnancy may serve as reprogramming strategies to reverse programming processes and prevent NCDs. In this review, firstly we summarize epidemiological evidence for nutritional programming of human disease. It will also discuss evidence from animal models, for the common mechanisms underlying nutritional programming, and potential nutritional interventions used as reprogramming strategies.

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17

Cerf, Marlon. "High Fat Programming and Cardiovascular Disease." Medicina 54, no. 5 (November 13, 2018): 86. http://dx.doi.org/10.3390/medicina54050086.

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Programming is triggered through events during critical developmental phases that alter offspring health outcomes. High fat programming is defined as the maintenance on a high fat diet during fetal and/or early postnatal life that induces metabolic and physiological alterations that compromise health. The maternal nutritional status, including the dietary fatty acid composition, during gestation and/or lactation, are key determinants of fetal and postnatal development. A maternal high fat diet and obesity during gestation compromises the maternal metabolic state and, through high fat programming, presents an unfavorable intrauterine milieu for fetal growth and development thereby conferring adverse cardiac outcomes to offspring. Stressors on the heart, such as a maternal high fat diet and obesity, alter the expression of cardiac-specific factors that alter cardiac structure and function. The proper nutritional balance, including the fatty acid balance, particularly during developmental windows, are critical for maintaining cardiac structure, preserving cardiac function and enhancing the cardiac response to metabolic challenges.

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18

Yilmaz, Ozge, Hasan Yuksel, and A. Sonia Buist. "Fetal Programming: Lung Health and Disease." Turkish Thoracic Journal 22, no. 5 (October 15, 2021): 413–17. http://dx.doi.org/10.5152/turkthoracj.2021.0196.

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19

Padmanabhan, Vasantha, Rodolfo C. Cardoso, and Muraly Puttabyatappa. "Developmental Programming, a Pathway to Disease." Endocrinology 157, no. 4 (February 9, 2016): 1328–40. http://dx.doi.org/10.1210/en.2016-1003.

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Abstract Accumulating evidence suggests that insults occurring during the perinatal period alter the developmental trajectory of the fetus/offspring leading to long-term detrimental outcomes that often culminate in adult pathologies. These perinatal insults include maternal/fetal disease states, nutritional deficits/excess, stress, lifestyle choices, exposure to environmental chemicals, and medical interventions. In addition to reviewing the various insults that contribute to developmental programming and the benefits of animal models in addressing underlying mechanisms, this review focuses on the commonalities in disease outcomes stemming from various insults, the convergence of mechanistic pathways via which various insults can lead to common outcomes, and identifies the knowledge gaps in the field and future directions.

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20

Andersen, Stine Linding, Jørn Olsen, and Peter Laurberg. "Foetal programming by maternal thyroid disease." Clinical Endocrinology 83, no. 6 (March 13, 2015): 751–58. http://dx.doi.org/10.1111/cen.12744.

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21

Langley-Evans, Simon C. "Developmental programming of health and disease." Proceedings of the Nutrition Society 65, no. 1 (February 2006): 97–105. http://dx.doi.org/10.1079/pns2005478.

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The environment encountered in fetal and neonatal life exerts a profound influence on physiological function and risk of disease in adult life. Epidemiological evidence suggests that impaired fetal growth followed by rapid catch-up in infancy is a strong predictor of obesity, hypertension, non-insulin-dependent diabetes and CHD. Whilst these associations have been widely accepted to be the product of nutritional factors operating in pregnancy, evidence from human populations to support this assertion is scarce. Animal studies clearly demonstrate that there is a direct association between nutrient imbalance in fetal life and later disease states, including hypertension, diabetes, obesity and renal disease. These associations are independent of changes in fetal growth rates. Experimental studies examining the impact of micro- or macronutrient restriction and excess in rodent pregnancy provide clues to the mechanisms that link fetal nutrition to permanent physiological changes that promote disease. Exposure to glucocorticoids in early life appears to be an important consequence of nutrient imbalance and may lead to alterations in gene expression that have major effects on tissue development and function. Epigenetic mechanisms, including DNA methylation, may also be important processes in early-life programming.

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22

BARKER, D. J. P. "In utero programming of chronic disease." Clinical Science 95, no. 2 (August 1, 1998): 115. http://dx.doi.org/10.1042/cs19980019.

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23

Paes, S. T., C. F. Gonçalves, M. M. Terra, T. S. Fontoura, M. de O. Guerra, V. M. Peters, P. C. de F. Mathias, and A. E. Andreazzi. "Childhood obesity: a (re) programming disease?" Journal of Developmental Origins of Health and Disease 7, no. 3 (October 26, 2015): 231–36. http://dx.doi.org/10.1017/s2040174415007837.

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The aim of our article was to review the current literature on the effects of metabolic (re) programming on childhood obesity. PubMed/MEDLINE was the data source used to track the studies. Descriptors applied: children obesity, epigenetic, metabolic programming, exercise and nutrition. The focus was to analyze and discuss the international findings on the theme. The gathering of the papers was performed between June and August 2014. The search of articles with the descriptors used found 33.054 studies. In all, 5.709 studies were selected by crossing chosen keywords. Among these, after careful reading of the titles, 712 papers were considered potential as references. After applying inclusion/exclusion criteria, 50 studies were selected from 132 eligible abstracts. Most studies linked the development and treatment of obesity from epigenetically stimulated metabolic programming during the early stages of pregnancy and life. This review provides theoretical basis to the understanding that the programmed development of childhood obesity may be linked to early exposure to environmental factors, such as (nutrition and regular practice of exercise) and stimulus can epigenetically alter the modulation of the obesogenic metabolic behavior during pregnancy and the developmental stages of children and/or postpone the pathophysiologic disease stage to adulthood.

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24

BARKER, D. "Fetal programming of coronary heart disease." Trends in Endocrinology and Metabolism 13, no. 9 (November 1, 2002): 364–68. http://dx.doi.org/10.1016/s1043-2760(02)00689-6.

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25

Remacle, C., F. Bieswal, and B. Reusens. "Programming of obesity and cardiovascular disease." International Journal of Obesity 28, S3 (November 2004): S46—S53. http://dx.doi.org/10.1038/sj.ijo.0802800.

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26

Barker, D. J. P. "In utero programming of cardiovascular disease." Theriogenology 53, no. 2 (January 2000): 555–74. http://dx.doi.org/10.1016/s0093-691x(99)00258-7.

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27

Chong, Euming, and Ihor V. Yosypiv. "Developmental Programming of Hypertension and Kidney Disease." International Journal of Nephrology 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/760580.

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A growing body of evidence supports the concept that changes in the intrauterine milieu during “sensitive” periods of embryonic development or in infant diet after birth affect the developing individual, resulting in general health alterations later in life. This phenomenon is referred to as “developmental programming” or “developmental origins of health and disease.” The risk of developing late-onset diseases such as hypertension, chronic kidney disease (CKD), obesity or type 2 diabetes is increased in infants born prematurely at <37 weeks of gestation or in low birth weight (LBW) infants weighing <2,500 g at birth. Both genetic and environmental events contribute to the programming of subsequent risks of CKD and hypertension in premature or LBW individuals. A number of observations suggest that susceptibility to subsequent CKD and hypertension in premature or LBW infants is mediated, at least in part, by reduced nephron endowment. The major factors influencingin uteroenvironment that are associated with a low final nephron number include uteroplacental insufficiency, maternal low-protein diet, hyperglycemia, vitamin A deficiency, exposure to or interruption of endogenous glucocorticoids, and ethanol exposure. This paper discusses the effect of premature birth, LBW, intrauterine milieu, and infant feeding on the development of hypertension and renal disease in later life as well as examines the role of the kidney in developmental programming of hypertension and CKD.

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28

Thompson, Michael D., and Brian J. DeBosch. "Maternal Fructose Diet-Induced Developmental Programming." Nutrients 13, no. 9 (September 20, 2021): 3278. http://dx.doi.org/10.3390/nu13093278.

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Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention.

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29

Wagle Shukla, Aparna, Pam Zeilman, Hubert Fernandez, Jawad A. Bajwa, and Raja Mehanna. "DBS Programming: An Evolving Approach for Patients with Parkinson’s Disease." Parkinson's Disease 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/8492619.

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Deep brain stimulation (DBS) surgery is a well-established therapy for control of motor symptoms in Parkinson’s disease. Despite an appropriate targeting and an accurate placement of DBS lead, a thorough and efficient programming is critical for a successful clinical outcome. DBS programming is a time consuming and laborious manual process. The current approach involves use of general guidelines involving determination of the lead type, electrode configuration, impedance check, and battery check. However there are no validated and well-established programming protocols. In this review, we will discuss the current practice and the recent advances in DBS programming including the use of interleaving, fractionated current, directional steering of current, and the use of novel DBS pulses. These technological improvements are focused on achieving a more efficient control of clinical symptoms with the least possible side effects. Other promising advances include the introduction of computer guided programming which will likely impact the efficiency of programming for the clinicians and the possibility of remote Internet based programming which will improve access to DBS care for the patients.

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30

Hur, Suzy S. J., Jennifer E. Cropley, and Catherine M. Suter. "Paternal epigenetic programming: evolving metabolic disease risk." Journal of Molecular Endocrinology 58, no. 3 (April 2017): R159—R168. http://dx.doi.org/10.1530/jme-16-0236.

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Parental health or exposures can affect the lifetime health outcomes of offspring, independently of inherited genotypes. Such ‘epigenetic’ effects occur over a broad range of environmental stressors, including defects in parental metabolism. Although maternal metabolic effects are well documented, it has only recently been established that that there is also an independent paternal contribution to long-term metabolic health. Both paternal undernutrition and overnutrition can induce metabolic phenotypes in immediate offspring, and in some cases, the induced phenotype can affect multiple generations, implying inheritance of an acquired trait. The male lineage transmission of metabolic disease risk in these cases implicates a heritable factor carried by sperm. Sperm-based transmission provides a tractable system to interrogate heritable epigenetic factors influencing metabolism, and as detailed here, animal models of paternal programming have already provided some significant insights. Here, we review the evidence for paternal programming of metabolism in humans and animal models, and the available evidence on potential underlying mechanisms. Programming by paternal metabolism can be observed in multiple species across animal phyla, suggesting that this phenomenon may have a unique evolutionary significance.

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31

Cormier, Tom. "Exercise Programming for Nonalcoholic Fatty Liver Disease." Strength & Conditioning Journal 41, no. 4 (August 2019): 89–93. http://dx.doi.org/10.1519/ssc.0000000000000462.

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32

Khan, I. Y., L. Lakasing, L. Poston, and K. H. Nicolaides. "Fetal programming for adult disease: where next?" Journal of Maternal-Fetal & Neonatal Medicine 13, no. 5 (January 2003): 292–99. http://dx.doi.org/10.1080/jmf.13.5.292.299.

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33

Meyer, Kurt, and Lubo Zhang. "Fetal Programming of Cardiac Function and Disease." Reproductive Sciences 14, no. 3 (April 2007): 209–16. http://dx.doi.org/10.1177/1933719107302324.

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34

Ran, Taojing, Shuo Geng, and Liwu Li. "Neutrophil programming dynamics and its disease relevance." Science China Life Sciences 60, no. 11 (September 29, 2017): 1168–77. http://dx.doi.org/10.1007/s11427-017-9145-x.

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35

Langley-Evans, Simon C. "Nutritional programming of disease: unravelling the mechanism." Journal of Anatomy 215, no. 1 (July 2009): 36–51. http://dx.doi.org/10.1111/j.1469-7580.2008.00977.x.

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36

Lane, Robert H. "Fetal Programming, Epigenetics, and Adult Onset Disease." Clinics in Perinatology 41, no. 4 (December 2014): 815–31. http://dx.doi.org/10.1016/j.clp.2014.08.006.

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37

Reichetzeder, Christoph, Sulistyo Emantoko Dwi Putra, Jian Li, and Berthold Hocher. "Developmental Origins of Disease - Crisis Precipitates Change." Cellular Physiology and Biochemistry 39, no. 3 (2016): 919–38. http://dx.doi.org/10.1159/000447801.

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The concept of developmental origins of diseases has gained a huge interest in recent years and is a constantly emerging scientific field. First observations hereof originated from epidemiological studies, linking impaired birth outcomes to adult chronic, noncommunicable disease. By now there is a considerable amount of both epidemiological and experimental evidence highlighting the impact of early life events on later life disease susceptibility. Albeit far from being completely understood, more recent studies managed to elucidate underlying mechanisms, with epigenetics having become almost synonymous with developmental programming. The aim of this review was to give a comprehensive overview of various aspects and mechanisms of developmental origins of diseases. Starting from initial research foci mainly centered on a nutritionally impaired intrauterine environment, more recent findings such as postnatal nutrition, preterm birth, paternal programming and putative interventional approaches are summarized. The review outlines general underlying mechanisms and particularly discusses mechanistic explanations for sexual dimorphism in developmental programming. Furthermore, novel hypotheses are presented emphasizing a non-mendelian impact of parental genes on the offspring's phenotype.

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38

Giussani, D. A., and S. T. Davidge. "Developmental programming of cardiovascular disease by prenatal hypoxia." Journal of Developmental Origins of Health and Disease 4, no. 5 (April 18, 2013): 328–37. http://dx.doi.org/10.1017/s204017441300010x.

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It is now recognized that the quality of the fetal environment during early development is important in programming cardiovascular health and disease in later life. Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. However, in contrast to the extensive research effort on pregnancy affected by maternal nutrition or maternal stress, the contribution of pregnancy affected by fetal chronic hypoxia to developmental programming is only recently becoming delineated and established. This review discusses the increasing body of evidence supporting the programming of cardiac susceptibility to ischaemia and reperfusion (I/R) injury, of endothelial dysfunction in peripheral resistance circulations, and of indices of the metabolic syndrome in adult offspring of hypoxic pregnancy. An additional focus of the review is the identification of plausible mechanisms and the implementation of maternal and early life interventions to protect against adverse programming.

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39

Franco, Maria C. P., Vanessa Oliveira, Beatriz Ponzio, Marina Rangel, Zaira Palomino, and Frida Zaladek Gil. "Influence of Birth Weight on the Renal Development and Kidney Diseases in Adulthood: Experimental and Clinical Evidence." International Journal of Nephrology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/608025.

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Several clinical and experimental studies support the hypothesis that foetal programming is an important determinant of nephropathy, hypertension, coronary heart disease, and type 2 diabetes during adulthood. In this paper, the renal repercussions of foetal programming are emphasised, and the physiopathological mechanisms are discussed. The programming of renal diseases is detailed based on the findings of kidney development and functional parameters.

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40

Jones, Dean L., James G. Phillips, John L. Bradshaw, Robert Iansek, and Judy A. Bradshaw. "Programming of single movements in Parkinson's disease: Comparison with huntington's disease." Journal of Clinical and Experimental Neuropsychology 14, no. 5 (September 1992): 762–72. http://dx.doi.org/10.1080/01688639208402861.

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41

Hsu, Chien-Ning, Hong-Ren Yu, Julie Y. H. Chan, Kay L. H. Wu, Wei-Chia Lee, and You-Lin Tain. "The Impact of Gut Microbiome on Maternal Fructose Intake-Induced Developmental Programming of Adult Disease." Nutrients 14, no. 5 (February 28, 2022): 1031. http://dx.doi.org/10.3390/nu14051031.

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Excessive or insufficient maternal nutrition can influence fetal development and the susceptibility of offspring to adult disease. As eating a fructose-rich diet is becoming more common, the effects of maternal fructose intake on offspring health is of increasing relevance. The gut is required to process fructose, and a high-fructose diet can alter the gut microbiome, resulting in gut dysbiosis and metabolic disorders. Current evidence from animal models has revealed that maternal fructose consumption causes various components of metabolic syndrome in adult offspring, while little is known about how gut microbiome is implicated in fructose-induced developmental programming and the consequential risks for developing chronic disease in offspring. This review will first summarize the current evidence supporting the link between fructose and developmental programming of adult diseases. This will be followed by presenting how gut microbiota links to common mechanisms underlying fructose-induced developmental programming. We also provide an overview of the reprogramming effects of gut microbiota-targeted therapy on fructose-induced developmental programming and how this approach may prevent adult-onset disease. Using gut microbiota-targeted therapy to prevent maternal fructose diet-induced developmental programming, we have the potential to mitigate the global burden of fructose-related disorders.

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42

Kett, Michelle M., and Kate M. Denton. "Renal programming: cause for concern?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 4 (April 2011): R791—R803. http://dx.doi.org/10.1152/ajpregu.00791.2010.

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Development of the kidney can be altered in utero in response to a suboptimal environment. The intrarenal factors that have been most well characterized as being sensitive to programming events are kidney mass/nephron endowment, the renin-angiotensin system, tubular sodium handling, and the renal sympathetic nerves. Newborns that have been subjected to an adverse intrauterine environment may thus begin life at a distinct disadvantage, in terms of renal function, at a time when the kidney must take over the primary role for extracellular fluid homeostasis from the placenta. A poor beginning, causing renal programming, has been linked to increased risk of hypertension and renal disease in adulthood. However, although a cause for concern, increasingly, evidence demonstrates that renal programming is not a fait accompli in terms of future cardiovascular and renal disease. A greater understanding of postnatal renal maturation and the impact of secondary factors (genes, sex, diet, stress, and disease) on this process is required to predict which babies are at risk of increased cardiovascular and renal disease as adults and to be able to devise preventative measures.

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43

Albertoni Borghese, Maria Florencia, Lucas Humberto Oronel, Maria Del Carmen Ortiz, and Mónica Patricia Majowicz. "Hypertension and renal disease programming: focus on the early postnatal period." Clinical Science 136, no. 17 (September 2022): 1303–39. http://dx.doi.org/10.1042/cs20220293.

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Abstract The developmental origin of hypertension and renal disease is a concept highly supported by strong evidence coming from both human and animal studies. During development there are periods in which the organs are more vulnerable to stressors. Such periods of susceptibility are also called ‘sensitive windows of exposure’. It was shown that as earlier an adverse event occurs; the greater are the consequences for health impairment. However, evidence show that the postnatal period is also quite important for hypertension and renal disease programming, especially in rodents because they complete nephrogenesis postnatally, and it is also important during preterm human birth. Considering that the developing kidney is vulnerable to early-life stressors, renal programming is a key element in the developmental programming of hypertension and renal disease. The purpose of this review is to highlight the great number of studies, most of them performed in animal models, showing the broad range of stressors involved in hypertension and renal disease programming, with a particular focus on the stressors that occur during the early postnatal period. These stressors mainly include undernutrition or specific nutritional deficits, chronic behavioral stress, exposure to environmental chemicals, and pharmacological treatments that affect some important factors involved in renal physiology. We also discuss the common molecular mechanisms that are activated by the mentioned stressors and that promote the appearance of these adult diseases, with a brief description on some reprogramming strategies, which is a relatively new and promising field to treat or to prevent these diseases.

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44

Tain, You-Lin, Li-Tung Huang, and Chien-Ning Hsu. "Developmental Programming of Adult Disease: Reprogramming by Melatonin?" International Journal of Molecular Sciences 18, no. 2 (February 16, 2017): 426. http://dx.doi.org/10.3390/ijms18020426.

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45

Cowan, Chad. "Programming and reprogramming: new approaches for understanding disease." QScience Proceedings 2012, no. 1 (March 5, 2012): 11. http://dx.doi.org/10.5339/qproc.2012.stem.1.11.

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46

LANGLEY-EVANS, S. "Fetal programming of immune function and respiratory disease." Clinical Experimental Allergy 27, no. 12 (December 1997): 1377–79. http://dx.doi.org/10.1111/j.1365-2222.1997.tb02979.x.

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Barker, DJP. "Intrauterine programming of coronary heart disease and stroke." Acta Paediatrica 86, S423 (November 1997): 178–82. http://dx.doi.org/10.1111/j.1651-2227.1997.tb18408.x.

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Durstine, J. Larry, William A. Webster, Dawn W. Blackhurst, Pamela K. McCarter, and Tracey J. Cole. "HEART DISEASE REVERSAL AND CONVENTIONAL CARDIAC REHABILITATION PROGRAMMING." Journal of Cardiopulmonary Rehabilitation 14, no. 5 (September 1994): 339. http://dx.doi.org/10.1097/00008483-199409000-00047.

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STEWART, MICHAEL S., MARGARET J. R. HEERWAGEN, and JACOB E. FRIEDMAN. "Developmental Programming of Pediatric Nonalcoholic Fatty Liver Disease." Clinical Obstetrics and Gynecology 56, no. 3 (September 2013): 577–90. http://dx.doi.org/10.1097/grf.0b013e3182a09760.

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Weiss, P. "Programming of a movement sequence in Parkinson's disease." Brain 120, no. 1 (January 1, 1997): 91–102. http://dx.doi.org/10.1093/brain/120.1.91.

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