Journal articles: 'Premature ageing'

1

Villanueva, M. Teresa. "Slowing premature ageing." Nature Reviews Cancer 15, no. 5 (April 24, 2015): 259. http://dx.doi.org/10.1038/nrc3956.

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Joss, Nicola, J. Michael Boulton‐Jones, and Ian More. "Premature ageing and glomerulonephritis." Nephrology Dialysis Transplantation 16, no. 3 (March 1, 2001): 615–18. http://dx.doi.org/10.1093/ndt/16.3.615.

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Smith, Michael. "Premature Ageing: History and Biology." Journal of the Royal Society of Medicine 87, no. 7 (July 1994): 425–27. http://dx.doi.org/10.1177/014107689408700720.

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Biesalski, H. K., M. Berneburg, T. Grune, M. Kerscher, J. Krutmann, W. Raab, J. Reimann, T. Reuther, L. Robert, and T. Schwarz. "Oxidative and premature skin ageing." Experimental Dermatology 12, s3 (December 2003): 3–15. http://dx.doi.org/10.1111/j.0906-6705.2003.00148.x.

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Dokal, Inderjeet. "A disease of premature ageing." Lancet 358 (December 2001): S27. http://dx.doi.org/10.1016/s0140-6736(01)07040-4.

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Silverstein, Janet H. "Does diabetes cause premature AGEing?" Journal of Pediatrics 172 (May 2016): 1–4. http://dx.doi.org/10.1016/j.jpeds.2016.03.011.

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Testori, Alessandro. "Short telomere syndromes, premature ageing syndromes, and biological ageing." Hong Kong Medical Journal 26, no. 1 (January 22, 2020): 76–77. http://dx.doi.org/10.12809/hkmj187782.

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Lehmann, Alan. "Ageing: Repair and Transcription Keep Us from Premature Ageing." Current Biology 12, no. 16 (August 2002): R550—R551. http://dx.doi.org/10.1016/s0960-9822(02)01050-3.

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DYER, CHRISTOPHER A. E., and ALAN J. SINCLAIR. "The premature ageing syndromes: insights into the ageing process." Age and Ageing 27, no. 1 (1998): 73–80. http://dx.doi.org/10.1093/ageing/27.1.73.

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Swanton, Alexander, and Tim Child. "Reproduction and ovarian ageing." British Menopause Society Journal 11, no. 4 (December 1, 2005): 126–31. http://dx.doi.org/10.1258/136218005775544200.

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Female fertility rates are inherently linked to a woman's age, which is in turn related to ovarian function. Reproductive potential declines gradually until 37–38 years of age, from when the rate of decline hastens. Approximately 1% of women suffer from premature ovarian ageing, and many may not have completed their families. This paper reviews the physiology and fertility consequences of ovarian ageing, premature ovarian failure, measures of ovarian reserve and methods of fertility preservation.

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Bhimani, Bhagyashri, Ankita Viroja, and D. V. Patel. "PREMATURE AGEING (AKALAJA JARA): AYURVEDIC VIEW." Journal of Biological & Scientific Opinion 4, no. 1 (March 16, 2016): 26–28. http://dx.doi.org/10.7897/2321-6328.0417.

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Coppede, Fabio. "Mutations Involved in Premature-Ageing Syndromes." Application of Clinical Genetics Volume 14 (June 2021): 279–95. http://dx.doi.org/10.2147/tacg.s273525.

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Kooman, Jeroen P., Peter Kotanko, Annemie M. W. J. Schols, Paul G. Shiels, and Peter Stenvinkel. "Chronic kidney disease and premature ageing." Nature Reviews Nephrology 10, no. 12 (October 7, 2014): 732–42. http://dx.doi.org/10.1038/nrneph.2014.185.

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MacNee, W. "Premature vascular ageing in cystic fibrosis." European Respiratory Journal 34, no. 6 (November 30, 2009): 1217–18. http://dx.doi.org/10.1183/09031936.00155209.

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Andressoo, J. O., and J. H. J. Hoeijmakers. "Transcription-coupled repair and premature ageing." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 577, no. 1-2 (September 2005): 179–94. http://dx.doi.org/10.1016/j.mrfmmm.2005.04.004.

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Jones, Bryony. "Heterochromatin disorganization associated with premature ageing." Nature Reviews Genetics 16, no. 6 (May 18, 2015): 318. http://dx.doi.org/10.1038/nrg3958.

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Cenni, Vittoria, Maria Rosaria D’Apice, Paolo Garagnani, Marta Columbaro, Giuseppe Novelli, Claudio Franceschi, and Giovanna Lattanzi. "Mandibuloacral dysplasia: A premature ageing disease with aspects of physiological ageing." Ageing Research Reviews 42 (March 2018): 1–13. http://dx.doi.org/10.1016/j.arr.2017.12.001.

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Sauzéat, Lucie, Anne Laurençon, and Vincent Balter. "Metallome evolution in ageing C. elegans and a copper stable isotope perspective." Metallomics 10, no. 3 (2018): 496–503. http://dx.doi.org/10.1039/c7mt00318h.

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O'Neill, Mary, Fatima Núñez, and David W. Melton. "p53 and a human premature ageing disorder." Mechanisms of Ageing and Development 124, no. 5 (May 2003): 599–603. http://dx.doi.org/10.1016/s0047-6374(03)00007-1.

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Toussaint, Olivier, Véronique Royer, Michel Salmon, and José Remacle. "Stress-induced premature senescence and tissue ageing." Biochemical Pharmacology 64, no. 5-6 (September 2002): 1007–9. http://dx.doi.org/10.1016/s0006-2952(02)01170-x.

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Stewart, Colin L., Alex Chojnowski, Rafidah Mutalif, Esther Wong, and Oliver Dreesen. "Premature ageing mutations at the nuclear periphery." Mechanisms of Development 145 (July 2017): S3. http://dx.doi.org/10.1016/j.mod.2017.04.521.

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Caravia, Xurde M., David Roiz-Valle, Alba Morán-Álvarez, and Carlos López-Otín. "Functional relevance of miRNAs in premature ageing." Mechanisms of Ageing and Development 168 (December 2017): 10–19. http://dx.doi.org/10.1016/j.mad.2017.05.003.

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Hull, J., R. Garrod, T. Ho, R. Knight, J. Cockcroft, D. Shale, and C. Bolton. "P2.08 PREMATURE VASCULAR AGEING IN CYSTIC FIBROSIS?" Artery Research 2, no. 3 (2008): 108. http://dx.doi.org/10.1016/j.artres.2008.08.374.

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De la Fuente, Mónica. "Murine models of premature ageing for the study of diet-induced immune changes: improvement of leucocyte functions in two strains of old prematurely ageing mice by dietary supplementation with sulphur-containing antioxidants." Proceedings of the Nutrition Society 69, no. 4 (September 28, 2010): 651–59. http://dx.doi.org/10.1017/s0029665110003848.

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Several immune functions are markers of health, biological age and predictors of longevity. A chronic oxidative and inflammatory state is the main cause of ageing and the immune system is involved in the rate of ageing. Thus, several murine models of premature ageing have been proposed owing to their early immunosenescence and oxidative stress, such as ovariectomised rats and mice, obese rats and anxious mice. In the last model, the most extensively studied by us, mice showing anxiety have an aged immune function and redox status as well as a shorter longevity in comparison with animals without anxiety of the same chronological age, being denominated prematurely ageing mice. A confirmation of the above is that the administration of diets supplemented with antioxidants improves the redox status and immune functions and increases the longevity of prematurely ageing mice. Antioxidant precursors of glutathione such as thioproline or N-acetylcysteine, which have a relevant role in ageing, have been the most widely investigated in adult prematurely ageing mice in our laboratory. In the present work, we have studied the effects of the ingestion for 5 weeks of a diet supplemented with 0·1% (w/w) thioproline+N-acetylcysteine on several functions of leucocytes from chronological old (69–73 weeks of age) prematurely ageing mice of two strains (Swiss and BALB/c). The results show an improvement of the immune functions, with their values becoming closer to those in adult animals (24±2 weeks). Thus, an adequate nutrition with antioxidants, even in aged subjects, could be a good strategy to retard ageing.

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WALLIS, CORRIN V., and RICHARD G. A. FARAGHER. "Telomeres, Telomerase, and Premature Aging." Journal of Anti-Aging Medicine 3, no. 4 (January 2000): 365–72. http://dx.doi.org/10.1089/rej.1.2000.3.365.

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E. Bauer, Moisés. "Premature immunosenescence: role of stress-related factors." PNEI REVIEW, no. 2 (November 2021): 20–33. http://dx.doi.org/10.3280/pnei2021-002003.

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The ageing of the immune system, immunosenescence, is associated with important remodelling changes in all lymphoid organs and its cells. However, the pace of ageing differs between people with the same chronological age, indicating that it may be thus influenced by extrinsic factors, including the chronic stress. In fact, young adults under chronic psychosocial stress may present immunosenescence features similarly to those found in older adults. Immunosenescence contributes to the onset and clinical course of age-related diseases such as neurodegenerative disorders, cancer, rheumatoid arthritis, cardiovascular and metabolic diseases. This article reviews that premature immunosenescence is observed in adults under chronic psychological stress as well as in healthy adolescents with history of childhood maltreatment. Superimposing stress during ageing is associated with further decline in adaptive immunity, increased inflammaging, accelerated cellular senescence and increased susceptibility to infections. This is of great interest for the COVID-19 pandemic, making the chronically stressed older adults of particular risk for worsen disease outcomes and poor vaccine responses.

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Kubben, Nard, and Tom Misteli. "Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases." Nature Reviews Molecular Cell Biology 18, no. 10 (August 9, 2017): 595–609. http://dx.doi.org/10.1038/nrm.2017.68.

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Yu, Xin, Quantao Liu, Pei Wan, Jiangkai Song, Huan Wang, Feiyang Zhao, Yafei Wang, and Jinyi Wu. "Effect of Ageing on Self-Healing Properties of Asphalt Concrete Containing Calcium Alginate/Attapulgite Composite Capsules." Materials 15, no. 4 (February 14, 2022): 1414. http://dx.doi.org/10.3390/ma15041414.

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Calcium alginate capsules within asphalt concrete can gradually release interior asphalt rejuvenator under cyclic loading to repair micro cracks and rejuvenate aged asphalt in-situ. However, asphalt pavement will become aged due to environmental and traffic factors during the service period. In view of this, this paper investigated the effect of ageing on the healing properties of asphalt concrete containing calcium alginate/attapulgite composite capsules under cyclic loading. The capsules were fabricated using the orifice-bath method and the morphological structure, mechanical strength, thermal stability, oil release ratios and healing levels of capsules in fresh, short-term ageing and long-term ageing asphalt concrete were explored. The results indicated that the different ageing treatments would not damage the multi-chamber structure nor decrease the mechanical strength of capsules but would induce the capsules release oil prematurely. The premature oil released from capsules in turn can offset the ageing effect owing to ageing treatment. The short-term ageing and long-term ageing plain asphalt mixtures gained strength recovery ratios of 39.3% and 34.2% after 64,000 cycles of compression loading, while the strength recovery ratios of short-term ageing and long-term ageing asphalt mixtures containing capsules were 63.5% and 54.8%, respectively.

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Harte, Alison L., Nancy F. da Silva, Michelle A. Miller, Francesco P. Cappuccio, Ann Kelly, Joseph P. O’Hare, Anthony H. Barnett, et al. "Telomere Length Attrition, a Marker of Biological Senescence, Is Inversely Correlated with Triglycerides and Cholesterol in South Asian Males with Type 2 Diabetes Mellitus." Experimental Diabetes Research 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/895185.

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South Asians have a higher risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) than white Caucasians, for a given BMI. Premature biological ageing, assessed by reduction in telomere length (TL), may be mediated by factors resulting from altered metabolic profiles associated with obesity. We hypothesise that ethnicity and metabolic status represent detrimental factors contributing to premature biological ageing. Therefore we assessed TL in two South Asian, age and BMI-matched cohorts [T2DM (n=142) versus non-T2DM (n=76)] to determine the effects of BMI, gender, lipid and CVD profile on biological ageing. Genomic DNA was obtained from the UKADS cohort; biochemical and anthropometric data was collected and TL was measured by quantitative real-time PCR. Our findings indicated a gender-specific effect with reduced TL in T2DM men compared with non-T2DM men (P=0.006). Additionally, in T2DM men, TL was inversely correlated with triglycerides and total cholesterol (r=−0.419,P<0.01;r=−0.443,P<0.01). In summary, TL was reduced amongst South Asian T2DM men and correlated with triglycerides and total cholesterol. This study highlights enhanced biological ageing among South Asian, T2DM men, which appears to be tracked by changes in lipids and BMI, suggesting that raised lipids and BMI may directly contribute to premature ageing.

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Roushan, Rakesh. "Association of Self Perception of Pre-Mature Ageing and Human Constitution (Prakriti) - A Cross-Sectional Study." Epidemiology International 7, no. 4 (December 31, 2022): 5–11. http://dx.doi.org/10.24321/2455.7048.202214.

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Introduction: Premature ageing is a process associated with a progressive accumulation of deleterious changes over time, an impairment of physiologic functions, an increase in the risk of disease and death. In Ayurveda, all human beings are categorised into basic sub-seven types based on their constitution. Along with this, ageing can be accelerated by lifestyle choices and environmental conditions to which our genes are exposed. The primary objective of the cross-sectional analysis was to find the association between prakriti and self-perception of premature ageing. Methodology: For the present study, a total of 100 participants, who were found positive for self-perception of pre-mature ageing and were fulfilling the other inclusion criteria, were eligible. The analysis of self-perception of pre-mature ageing was done by using The Brief Ageing Perception Questionnaire (B-APQ). The assessment of prakriti was done with a validated Prakriti Analysis Pro forma prepared by the Central Council for Research in Ayurvedic Sciences (CCRAS), New Delhi, India. Result: The prevalence of self-perception of pre-mature ageing was maximum among vata prakriti (58, 58%) and minimum in kapha prakriti (18, 18%). A significant association of male and female participants was found with three questions of B-APQ by applying Fisher Exact test. No significant association was found between the group of vata, pitta and kapha dominant prakriti with individual B-APQ on applying independent-samples Kruskal-Wallis test. As per descriptive analysis, vata prakriti individuals were more vulnerable to the self-perception of premature ageing as per B-APQ while kapha prakriti was the least. The distribution of individual B-APQ was the same across all categories of prakriti.

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Albarrati, A., N. Gale, S. Enright, M. Munnery, I. Munnery, S. Saikia, J. Cockcroft, and D. Shale. "M139 Frailty And Premature Cardiovascular Ageing In Copd." Thorax 69, Suppl 2 (November 10, 2014): A212—A213. http://dx.doi.org/10.1136/thoraxjnl-2014-206260.434.

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Uziel, Orit, Meir Lahav, Liat Shargian, Einat Beery, Oren Pasvolsky, Uri Rozovski, Pia Raanani, and Moshe Yeshurun. "Premature ageing following allogeneic hematopoietic stem cell transplantation." Bone Marrow Transplantation 55, no. 7 (February 24, 2020): 1438–46. http://dx.doi.org/10.1038/s41409-020-0839-z.

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33

Wood, Heather. "Premature cellular ageing limits remyelination in progressive MS." Nature Reviews Neurology 15, no. 6 (April 9, 2019): 309. http://dx.doi.org/10.1038/s41582-019-0187-z.

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Cupit-Link, Margaret C., James L. Kirkland, Kirsten K. Ness, Gregory T. Armstrong, Tamar Tchkonia, Nathan K. LeBrasseur, Saro H. Armenian, Kathryn J. Ruddy, and Shahrukh K. Hashmi. "Biology of premature ageing in survivors of cancer." ESMO Open 2, no. 5 (November 2017): e000250. http://dx.doi.org/10.1136/esmoopen-2017-000250.

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Hamzelou, Jessica. "Italy's ‘triangle of Death’ linked to premature ageing." New Scientist 214, no. 2860 (April 2012): 10. http://dx.doi.org/10.1016/s0262-4079(12)60934-8.

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Morocutti, A., K. A. Earle, H. P. Rodemann, and G. C. Viberti. "Premature cell ageing and evolution of diabetic nephropathy." Diabetologia 40, no. 2 (January 28, 1997): 244–46. http://dx.doi.org/10.1007/s001250050670.

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Ebert, Thomas, Sven-Christian Pawelzik, Anna Witasp, Samsul Arefin, Sam Hobson, Karolina Kublickiene, Paul G. Shiels, Magnus Bäck, and Peter Stenvinkel. "Inflammation and Premature Ageing in Chronic Kidney Disease." Toxins 12, no. 4 (April 4, 2020): 227. http://dx.doi.org/10.3390/toxins12040227.

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Persistent low-grade inflammation and premature ageing are hallmarks of the uremic phenotype and contribute to impaired health status, reduced quality of life, and premature mortality in chronic kidney disease (CKD). Because there is a huge global burden of disease due to CKD, treatment strategies targeting inflammation and premature ageing in CKD are of particular interest. Several distinct features of the uremic phenotype may represent potential treatment options to attenuate the risk of progression and poor outcome in CKD. The nuclear factor erythroid 2-related factor 2 (NRF2)–kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (KEAP1) signaling pathway, the endocrine phosphate-fibroblast growth factor-23–klotho axis, increased cellular senescence, and impaired mitochondrial biogenesis are currently the most promising candidates, and different pharmaceutical compounds are already under evaluation. If studies in humans show beneficial effects, carefully phenotyped patients with CKD can benefit from them.

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Kooman, Jeroen P., Peter Stenvinkel, and Paul G. Shiels. "Fabry Disease: A New Model of Premature Ageing?" Nephron 144, no. 1 (September 27, 2019): 1–4. http://dx.doi.org/10.1159/000503290.

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Martens, Dries S., Harald Mischak, Tim S. Nawrot, and Jan A. Staessen. "A urinary proteomic marker indicative of premature ageing." Blood Pressure Monitoring 27, Suppl 1 (November 25, 2022): e9-e9. http://dx.doi.org/10.1097/01.mbp.0000905240.53184.3c.

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Zhang, Kexiong, Lihui Wang, Xiaojing Hong, Hao Chen, Yao Shi, Yingying Liu, Jun Liu, and Jun-Ping Liu. "Pulmonary Alveolar Stem Cell Senescence, Apoptosis, and Differentiation by p53-Dependent and -Independent Mechanisms in Telomerase-Deficient Mice." Cells 10, no. 11 (October 26, 2021): 2892. http://dx.doi.org/10.3390/cells10112892.

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Pulmonary premature ageing and fibrogenesis as in idiopathic pulmonary fibrosis (IPF) occur with the DNA damage response in lungs deficient of telomerase. The molecular mechanism mediating pulmonary alveolar cell fates remains to be investigated. The present study shows that naturally occurring ageing is associated with the DNA damage response (DDR) and activation of the p53 signalling pathway. Telomerase deficiency induced by telomerase RNA component (TERC) knockout (KO) accelerates not only replicative senescence but also altered differentiation and apoptosis of the pulmonary alveolar stem cells (AEC2) in association with increased innate immune natural killer (NK) cells in TERC KO mice. TERC KO results in increased senescence-associated heterochromatin foci (SAHF) marker HP1γ, p21, p16, and apoptosis-associated cleaved caspase-3 in AEC2. However, additional deficiency of the tumour suppressor p53 in the Trp53−/− allele of the late generation of TERC KO mice attenuates the increased senescent and apoptotic markers significantly. Moreover, p53 deficiency has no significant effect on the increased gene expression of T1α (a marker of terminal differentiated AEC1) in AEC2 of the late generation of TERC KO mice. These findings demonstrate that, in natural ageing or premature ageing accelerated by telomere shortening, pulmonary senescence and IPF develop with alveolar stem cell p53-dependent premature replicative senescence, apoptosis, and p53-independent differentiation, resulting in pulmonary senescence-associated low-grade inflammation (SALI). Our studies indicate a natural ageing-associated molecular mechanism of telomerase deficiency-induced telomere DDR and SALI in pulmonary ageing and IPF.

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Li, Zirui, Zhiqiang Chen, Lianghao Zhao, Jiaqi Sun, Lin Yin, Yuwei Jiang, Xiaotong Shi, Ziye Song, and Lu Zhang. "Lack of T04C9.1, the Homologue of Mammalian APPL2, Leads to Premature Ageing and Shortens Lifespan in Caenorhabditis elegans." Genes 15, no. 6 (May 22, 2024): 659. http://dx.doi.org/10.3390/genes15060659.

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Ageing has been identified as an independent risk factor for various diseases; however, the physiological basis and molecular changes related to ageing are still largely unknown. Here, we show that the level of APPL2, an adaptor protein, is significantly reduced in the major organs of aged mice. Knocking down APPL2 causes premature ageing of human umbilical vein endothelial cells (HUVECs). We find that a lack of T04C9.1, the homologue of mammalian APPL2, leads to premature ageing, slow movements, lipid deposition, decreased resistance to stresses, and shortened lifespan in Caenorhabditis elegans (C. elegans), which are associated with decreased autophagy. Activating autophagy by rapamycin or inhibition of let-363 suppresses the age-related alternations, impaired motility, and shortened lifespan of C. elegans, which are reversed by knocking down autophagy-related genes. Our work provides evidence that APPL2 and its C. elegans homologue T04C9.1 decrease with age and reveals that a lack of T04C9.1 bridges autophagy decline and ageing in C. elegans.

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Tsunoda, Koichi, Minako Takanosawa, Yukiko Kurikawa, Kenji Nosaka, and Seiji Niimi. "Hoarse voice resulting from premature ageing in Werner’s syndrome." Journal of Laryngology & Otology 114, no. 1 (January 2000): 61–63. http://dx.doi.org/10.1258/0022215001903708.

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Werner’s syndrome is characterized by clinical signs of premature ageing. A 42-year-old man presented with three-year history of hoarseness. Also noted were skin atrophy of the face and hands, ulcerations around the ankles, and a history of cataracts. A clinical diagnosis of Werner’s syndrome was made. Laryngoscopy revealed bowed vocal folds resulting in a spindle-shaped defect with glottal incompetence during phonation. Examination also revealed decreased maximum phonation time and vocal fatigue. At surgery, atrophy of the vocalis muscle was noted. Furthermore, degeneration of muscle fibres was noted in the temporalis muscle. The atrophic changes in the vocal folds that occur with ageing and result in an increased fundamental frequency were seen in this patient. The characteristic hoarseness of Werner’s syndrome appears to be the result of premature ageing of the vocal folds.

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Manna, Samprikta, Cathal McCarthy, and Fergus P. McCarthy. "Placental Ageing in Adverse Pregnancy Outcomes: Telomere Shortening, Cell Senescence, and Mitochondrial Dysfunction." Oxidative Medicine and Cellular Longevity 2019 (May 22, 2019): 1–11. http://dx.doi.org/10.1155/2019/3095383.

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Preeclampsia is a multisystemic pregnancy disorder and a major cause of maternal and neonatal morbidity and mortality worldwide. The exact pathophysiology of preeclampsia remains unclear; however, it is speculated that the various pathologies can be attributed to impaired vascular remodelling and elevated oxidative stress within the placenta. Oxidative stress plays a key role in cell ageing, and the persistent presence of elevated oxidative stress precipitates cellular senescence and mitochondrial dysfunction, resulting in premature ageing of the placenta. Premature ageing of the placenta is associated with placental insufficiency, which reduces the functional capacity of this critical organ and leads to abnormal pregnancy outcomes. The changes brought about by oxidative insults are irreversible and often lead to deleterious modifications in macromolecules such as lipids and proteins, DNA mutations, and alteration of mitochondrial functioning and dynamics. In this review, we have summarized the current knowledge of placental ageing in the aetiology of adverse pregnancy outcomes and discussed the hallmarks of ageing which could be potential markers for preeclampsia and fetal growth restriction.

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Anisimov, Vladimir. "Premature Ageing Prevention: Limitations and Perspectives of Pharmacological Interventions." Current Drug Targets 7, no. 11 (November 1, 2006): 1485–503. http://dx.doi.org/10.2174/1389450110607011485.

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Varshney, Iti, Mohammad Adil, Syed Suhail Amin, Mohd Mohtashim, Annu Priya, and Mahtab Alam. "Hutchinson-Gilford progeria syndrome: a rare premature ageing syndrome." Dermatology Review 107, no. 2 (2020): 179–83. http://dx.doi.org/10.5114/dr.2020.96361.

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Pashinyan, A. G., S. A. Heidar, G. B. Arutyunyan, and Ye V. Dontsova. "Skin moisturizing as a factor preventing premature skin ageing." Vestnik dermatologii i venerologii 89, no. 4 (August 15, 2013): 104–7. http://dx.doi.org/10.25208/vdv634.

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The authors describe issues related to age-related changes in the skin. They present data confirming the clinical efficacy of hydration cosmetic drugs belonging to the Noreva Aquareva line by Laboratoires Dermatologiques d’Uriage aimed at renewing the natural moisture-preserving epidermis structure in patients with dry skin within a short period of time.

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&NA;. "PUVA may induce premature ageing and nonmelanoma skin cancers." Reactions Weekly &NA;, no. 313 (August 1990): 3. http://dx.doi.org/10.2165/00128415-199003130-00006.

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Green, Adèle C. "Premature ageing of the skin in a Queensland population." Medical Journal of Australia 155, no. 7 (October 1991): 473–78. http://dx.doi.org/10.5694/j.1326-5377.1991.tb93845.x.

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Dotti, Maria Teresa, Gerald Salen, and Antonio Federico. "Cerebrotendinous Xanthomatous as a Multisystem Disease Mimicking Premature Ageing." Developmental Neuroscience 13, no. 4-5 (1991): 371–76. http://dx.doi.org/10.1159/000112187.

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Trifunovic, Aleksandra, Anna Wredenberg, Maria Falkenberg, Johannes N. Spelbrink, Anja T. Rovio, Carl E. Bruder, Mohammad Bohlooly-Y, et al. "Premature ageing in mice expressing defective mitochondrial DNA polymerase." Nature 429, no. 6990 (May 2004): 417–23. http://dx.doi.org/10.1038/nature02517.

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Journal articles on the topic 'Premature ageing'

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