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1

Subramanian, Geetha, Balaji Lohiya, and Dharmendra Jain. "Sex Hormones and Cardiovascular Diseases." Journal of Cardiovascular Medicine and Surgery 3, no. 2 (2017): 198–201. http://dx.doi.org/10.21088/jcms.2454.7123.3217.19.

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2

Basit Ashraf, Muhammad Abdul, Razia Rizwan, Mahwish Arooj, Arif Malik, and Sarmad Bashir. "CARDIOVASCULAR DISEASES." Professional Medical Journal 23, no. 11 (November 10, 2016): 1400–1411. http://dx.doi.org/10.29309/tpmj/2016.23.11.1770.

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Background: Atherosclerosis, with chief contribution of vascular injury,inflammation and oxidative stress is the major cause of majority of cardiovascular diseases.Understanding of its pathophysiology provides initial prognosis, designing of new therapeuticsfor its prevention and different treatment protocols. Objectives: The present study wasdesigned to evaluate the role of oxidative and inflammatory markers of medical importancein the development of cardiovascular diseases. Study Design: Prospective case controlstudy. Setting: Sample collection from Punjab Institute of Cardiology (PIC), Lahore and allthe experimental work was done at Institute of Molecular Biology and Biotechnology (IMBB),The University of Lahore. Period: February 2015 to April 2016. Methodology: Biophysical,hematological, antioxidative capacity, inflammatory markers and lipid profile were estimatedin atherosclerotic patients. Results: The BMI (31.26±1.66) were significantly increased inatherosclerotic patients when were compared with controls. MDA was recorded as 3.99±0.16in atherosclerotic patients followed by 1.66±0.11 nmol/ml in healthy control respectively. Nitricoxide (NO) in the patients (35.26±4.26 ng/ml) was also significantly raised in the patientsthan normal subjects (21.26±2.35 ng/ml). Whereas mean serum levels of MPO and AGEsin patients were 0.237±.0013 pmol/ml and 2.46±0.09 U/ml respectively. Increased levels ofTCh (217.56±10.99, TG (199.67±11.02), and LDL (131.87±9.56) along with decrease in HDL33.76±3.85 mg/dl were recorded respectively. The hs-CRP showed significant increased levelsin atherosclerotic group (3.93±0.14mg/dl) as compared to normal control (1.68±0.06mg/L).The mean serum level of TNF-α and IL-6 in diseased group was recorded as 41.25±3.65pg/mland 6.35±0.64 pg/ml respectively. The significant decreasing trend of total anti-oxidant capacity,SOD, CAT, GSH, GPx, GRx, vitamin A and C but increasing drift of vitamin E was observed inatherosclerotic patients. Conclusion: Following study reported that elevated oxidative stressand inflammation along with lipid peroxidation are the major contributors in the progression ofatherosclerosis.
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3

Bognolo, G. "Cardiovascular diseases." BMJ 327, no. 7427 (December 6, 2003): 1354—a—1354. http://dx.doi.org/10.1136/bmj.327.7427.1354-a.

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4

Archer, L. Nicholas J. "Cardiovascular diseases." Current Opinion in Pediatrics 2, no. 1 (February 1990): 91–94. http://dx.doi.org/10.1097/00008480-199002000-00017.

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5

FLACK, J. "Cardiovascular diseases." American Journal of Hypertension 10, no. 4 (April 1997): 227A. http://dx.doi.org/10.1016/s0895-7061(97)89485-x.

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6

Kakkar, Rahul, and Richard T. Lee. "Cardiovascular diseases." Drug Discovery Today: Disease Models 4, no. 4 (December 2007): 163–64. http://dx.doi.org/10.1016/j.ddmod.2008.04.001.

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7

Macphee, Colin H., and Alan Daugherty. "Cardiovascular diseases." Drug Discovery Today: Therapeutic Strategies 5, no. 1 (March 2008): 1–3. http://dx.doi.org/10.1016/j.ddstr.2008.11.002.

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8

Alpert, Joseph S. "Cardiovascular Diseases." JAMA: The Journal of the American Medical Association 254, no. 16 (October 25, 1985): 2264. http://dx.doi.org/10.1001/jama.1985.03360160096020.

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9

Viera, Anthony J. "Cardiovascular Diseases." Primary Care: Clinics in Office Practice 51, no. 1 (March 2024): i. http://dx.doi.org/10.1016/s0095-4543(23)00109-4.

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10

Aslam, Dr Imran, Yuldashev Soatboy Jiyanboyevich, and Abdurakhmanova Zamira Ergashboevna. "Prevention & Treatment Of Cardiovascular Diseases." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 06 (June 10, 2021): 180–88. http://dx.doi.org/10.37547/tajmspr/volume03issue06-28.

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Cardiovascular disease is a significant problem that humans have always faced, affecting thousands of people's lives and health and taking the lives of many people. Many medical institutions and researchers have regarded it as a significant problem in overcoming the cardiovascular disease.1 Much attention has been paid, so the prevention and treatment level in this area has also been rapidly improved. However, cardiovascular disease still cannot be prevented or treated fundamentally, and it is still a significant danger to human health. All people still hope for breakthrough results in cardiovascular disease.2 This article analyzes the prevention and treatment of cardiovascular diseases, and has obtained a series of practical and reliable conclusions.
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11

deBerrazueta-Fernández, José Ramón. "Aging and Cardiovascular Diseases." ANALES RANM 135, no. 03 (January 2, 2019): 266–80. http://dx.doi.org/10.32440/ar.2018.135.03.rev09.

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12

Ninomiya, Toshiharu, and Yutaka Kiyohara. "1. Cardiovascular Diseases." Nihon Naika Gakkai Zasshi 96, no. 5 (2007): 887–93. http://dx.doi.org/10.2169/naika.96.887.

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13

Takahashi, Nobuyuki, Tadafumi Doi, and Tetsuro Sugiura. "2. Cardiovascular Diseases." Nihon Naika Gakkai Zasshi 97, no. 12 (2008): 2936–42. http://dx.doi.org/10.2169/naika.97.2936.

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14

Deac, Radu. "Cardiovascular diseases management." Management in Health XIII, no. 4 (December 30, 2009): 1–2. http://dx.doi.org/10.5233/mih.2009.0023.

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15

Sone, Hiroto, and Nobuhiro Yamada. "5. Cardiovascular Diseases." Nihon Naika Gakkai Zasshi 98, no. 4 (2009): 794–801. http://dx.doi.org/10.2169/naika.98.794.

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16

Limongelli, Giuseppe, Emanuele Monda, Michele Lioncino, and Eduardo Bossone. "Rare Cardiovascular Diseases." Heart Failure Clinics 18, no. 1 (January 2022): i. http://dx.doi.org/10.1016/s1551-7136(21)00101-x.

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17

Podolec, Piotr. "Rare cardiovascular diseases." European Heart Journal 38, no. 43 (November 14, 2017): 3190–92. http://dx.doi.org/10.1093/eurheartj/ehx611.

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18

Janssens, U. "Septic cardiovascular diseases." DMW - Deutsche Medizinische Wochenschrift 128, no. 15 (April 2003): 803–9. http://dx.doi.org/10.1055/s-2003-38586.

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19

Seward, James B., and Grace Casaclang-Verzosa. "Infiltrative Cardiovascular Diseases." Journal of the American College of Cardiology 55, no. 17 (April 2010): 1769–79. http://dx.doi.org/10.1016/j.jacc.2009.12.040.

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20

Kumar, Raman Krishna, Valentin Fuster, and Dorairaj Prabhakaran. "Tropical Cardiovascular Diseases." Journal of the American College of Cardiology 81, no. 1 (January 2023): 68–70. http://dx.doi.org/10.1016/j.jacc.2022.11.003.

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21

Kadirovna, Muratova Saodat, Shukurova Nodira Tillayevna, Baratov Bobur, and Teshayev Shoxjahon. "PREDICTIVE MODELING OF THE PROBABILITY OF DEVELOPING PERIODONTAL DISEASES IN PATIENTS WITH CARDIOVASCULAR DISEASE." European International Journal of Multidisciplinary Research and Management Studies 4, no. 4 (April 1, 2024): 65–70. http://dx.doi.org/10.55640/eijmrms-04-04-10.

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Currently, the forecast of the development of pathology is an important part of all branches of healthcare. [3,4,5]. However, despite the importance and scientific and practical significance of forecasting in dentistry, at present we have not found information about predictive models of individual risk of developing periodontitis in patients with hypertension.
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22

Hisatome, Ichiro, Peili Li, Fikri Taufiq, Nani Maharani, Masanari Kuwabara, Haruaki Ninomiya, and Udin Bahrudin. "Hyperuricemia as a Risk Factor for Cardiovascular Diseases." Journal of Biomedicine and Translational Research 6, no. 3 (December 23, 2020): 101–9. http://dx.doi.org/10.14710/jbtr.v6i3.9383.

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Serum uric acid level above 7 mg/dl is defined as hyperuricemia, which gives rise to the monosodium urate (MSU), causing gout and urolithiasis. Hyperuricemia is an independent risk factor as well as a marker for hypertension, heart failure, atherosclerosis, atrial fibrillation, and chronic kidney disease. MSU crystals, soluble uric acid (UA), or oxidative stress derived from xanthine oxidoreductase (XOR) might be plausible explanations for the association of cardio-renovascular diseases with hyperuricemia. In macrophages, MSU activates the Nod-like receptor family, pyrin domain containing 3(NLRP3) inflammasome, and proteolytic processing mediated by caspase-1 with enhanced interleukin (IL)-1β and IL-18 secretion. Soluble UA accumulates intracellularly through UA transporters (UAT) in vascular and atrial myocytes, causing endothelial dysfunction ad atrial electrical remodeling. XOR generates reactive oxygen species (ROS) that lead to cardiovascular diseases. Since it remains unclear whether asymptomatic hyperuricemia could be a risk factor for cardiovascular and kidney diseases, European and American guidelines do not recommend pharmacological treatment for asymptomatic patients with cardio-renovascular diseases. The Japanese guideline, on the contrary, recommends pharmacological treatment for hyperuricemia with CKD to protect renal function, and it attaches importance of the cardio-renal interaction for the treatment of asymptomatic hyperuricemia patients with hypertension and heart failure.
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23

George, Melvin, and Luxitaa Goenka. "Air Pollution and its Association with Cardiovascular Diseases." Journal of Cardiovascular Medicine and Surgery 4, no. 2 (2018): 176–82. http://dx.doi.org/10.21088/jcms.2454.7123.4218.18.

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24

Shakhnoza, Iskandarova, and Amilova Asalya. "CARDIOVASCULAR DISEASES AS A SOCIAL AND HYGIENIC PROBLEM." American Journal of Medical Sciences and Pharmaceutical Research 04, no. 04 (April 1, 2022): 25–27. http://dx.doi.org/10.37547/tajmspr/volume04issue04-07.

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Cardiovascular disease is the most important cause of death in the population. Enormous advances in prevention, diagnosis and treatment have comparatively reduced the incidence of the disease. Cardiovascular diseases remain the most important cause of early disability, occupational disability and premature death.
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25

Katerenchuk, O. "Depression аnd Cardiovascular Diseases: Cause, Consequence оr Comorbidity." Lviv clinical bulletin 3, no. 3 (September 16, 2013): 49–51. http://dx.doi.org/10.25040/lkv2013.03.049.

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26

Lin, Qiuzhen, Wanyun Zuo, Yaozhong Liu, Keke Wu, and Qiming Liu. "NAD+ and cardiovascular diseases." Clinica Chimica Acta 515 (April 2021): 104–10. http://dx.doi.org/10.1016/j.cca.2021.01.012.

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27

Sahil, MD, Nikita Tiwari, and Manleen Kaur. "Nutraceuticals In Cardiovascular Diseases." American Journal of Pharmacy And Health Research 9, no. 1 (January 25, 2021): 11–32. http://dx.doi.org/10.46624/ajphr.2021.v9.i1.002.

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28

Trivedi, Akhilesh, and Mohammed A. Hannan. "Radiation and Cardiovascular Diseases." Journal of Environmental Pathology, Toxicology and Oncology 23, no. 2 (2004): 99–106. http://dx.doi.org/10.1615/jenvpathtoxoncol.v23.i2.20.

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29

Agarwal, Shashi. "Depression and Cardiovascular Diseases." International Journal of Medical Science and Clinical Invention 8, no. 03 (March 28, 2021): 5302–16. http://dx.doi.org/10.18535/ijmsci/v8i03.08.

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Cardiovascular diseases (CVD) are the leading cause of global morbidity and mortality. Besides imparting enormous human suffering and enhancing premature mortality, they also inflict huge direct and indirect financial costs on the worldwide society. With the easier availability of affordable therapeutics globally, and the relatively paucity of newer innovations, modifiable risk factors are gaining greater importance in the management of this cardiovascular epidemic. Depression is a modifiable risk factor. It is consistently and strongly associated with a higher risk of CVD incidence and mortality. CVD on the other hand, often induces the development of depression. This paper reviews the effects of depression on cardiovascular diseases.
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30

Du, Sheng-Li, Zeng-Qin Jia, Jiu-Chang Zhong, and Le-Feng Wang. "TRPC5 in cardiovascular diseases." Reviews in Cardiovascular Medicine 22, no. 1 (2021): 127. http://dx.doi.org/10.31083/j.rcm.2021.01.212.

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31

Fares, Auda. "Winter cardiovascular diseases phenomenon." North American Journal of Medical Sciences 5, no. 4 (2013): 266. http://dx.doi.org/10.4103/1947-2714.110430.

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32

Greiffeneggová, Liana, and Drahoslava Hrubá. "Cardiovascular Diseases among Women." Hygiena 62, no. 1 (March 1, 2017): 18–23. http://dx.doi.org/10.21101/hygiena.a1494.

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33

Sherif, Abdulmagid, Mohamed Benhammuda, Serag Fares, and Terry L. Oroszi. "Cardiovascular Diseases and Radiations." Journal of Biosciences and Medicines 05, no. 02 (2017): 72–77. http://dx.doi.org/10.4236/jbm.2017.52007.

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34

Zhang, Gaigai, and Xinhua Yin. "Ghrelin and Cardiovascular Diseases." Current Cardiology Reviews 999, no. 999 (December 11, 2009): 1–8. http://dx.doi.org/10.2174/1573210ccr06017403x.

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35

Mohibullah, AKM. "Cardiovascular Diseases in Bangladesh." Cardiovascular Journal 9, no. 2 (May 8, 2017): 75–76. http://dx.doi.org/10.3329/cardio.v9i2.32416.

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36

Ikeda, Masao. "Cardiovascular diseases in Japan1." Clinical Hemorheology and Microcirculation 1, no. 3 (December 9, 2016): 327–29. http://dx.doi.org/10.3233/ch-1981-1313.

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37

Guieu, Régis, Jean Ruf, and Giovanna Mottola. "Hyperhomocysteinemia and cardiovascular diseases." Annales de Biologie Clinique 80, no. 1 (February 2022): 7–14. http://dx.doi.org/10.1684/abc.2021.1694.

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38

Fujii, Satoshi, Atsushi Ito, and Yumi Watanabe. "Biomarkers for Cardiovascular Diseases." Annals of Nuclear Cardiology 2, no. 1 (2016): 94–98. http://dx.doi.org/10.17996/anc.02.01.94.

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39

Fujii, Satoshi, Atsushi Ito, and Yumi Watanabe. "Biomarkers for Cardiovascular Diseases." Annals of Nuclear Cardiology 2, no. 1 (2016): 94–98. http://dx.doi.org/10.17996/anc.2.1_94.

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40

H, Song. "Lipid-induced cardiovascular diseases." Journal of Cardiology and Cardiovascular Medicine 2, no. 1 (2017): 085–94. http://dx.doi.org/10.29328/journal.jccm.1001018.

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41

Bonnefont-Rousselot, Dominique. "Resveratrol and Cardiovascular Diseases." Nutrients 8, no. 5 (May 2, 2016): 250. http://dx.doi.org/10.3390/nu8050250.

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42

Celeghin, Rudy, Gaetano Thiene, Barbara Bauce, Cristina Basso, and Kalliopi Pilichou. "Genetics in cardiovascular diseases." Italian Journal of Medicine 13, no. 3 (September 6, 2019): 137–51. http://dx.doi.org/10.4081/itjm.2019.1186.

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Cardiovascular diseases (CVDs) are a wide group of disorders affecting the heart and blood vessels, including coronary artery, valve, pericardial, conduction system, myocardial and vascular diseases, either congenital or acquired, which can be also heritable. The advent of next generation sequencing (NGS) was accompanied by quick advances in understanding the genetic basis of human diseases, prompting translation of genetics to the clinic. Precision medicine is based on these findings and on the role of genetic testing to improve the diagnosis, to identify individuals with previously unrecognized disease and family members at risk of future disease development which require longitudinal follow-up. However, the probabilistic nature of genetic testing and the subjectivity of genetic variants classification weighted on current evidence, making this powerful clinical tool difficult to be applied in precision diagnostics and therapeutics. Here, we reviewed systematically the genetic basis of CVDs with special emphasis on the current role of NGS in clinical diagnosis and risk assessment, underlying the need of multidisciplinary cardio-genetic referral centers.
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43

Stajic, Dalibor, and Nela Djonovic. "Cardiovascular diseases: Risk factors." Medicinski casopis 50, no. 2 (2016): 43–48. http://dx.doi.org/10.5937/mckg50-11761.

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44

Fukumoto, Yoshihiro. "Nutrition and Cardiovascular Diseases." Nutrients 14, no. 1 (December 27, 2021): 94. http://dx.doi.org/10.3390/nu14010094.

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45

Hu, Qinqin, Zheyan Fang, Junbo Ge, and Hua Li. "Nanotechnology for cardiovascular diseases." Innovation 3, no. 2 (March 2022): 100214. http://dx.doi.org/10.1016/j.xinn.2022.100214.

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46

Savić, Kristina, Sonja Zafirović, Ivana Resanović, Emina Sudar, Vera Maravić-Stojković, Biljana Putniković, and Esma Isenović. "Biomarkers of cardiovascular diseases." Medicinska istrazivanja 47, no. 2 (2013): 11–19. http://dx.doi.org/10.5937/medist1302011s.

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Biomarkers are indicators of normal biological processes, pathogenic processes or pharmacologic responses to therapeutic interventions. Interleukin-6 (IL - 6) is a biomarker whose synthesis could be activated by various stimuli, such as interferon-g (IFN - g), tumor necrosis factor (TNF) and/or interleukin - 1 (IL - 1). IL - 6 achieves its effects through the IL-6 receptor (IL - 6R). It has been shown that transgenic mice, which have induced expression of IL - 6 and IL - 6R develop myocardial hypertrophy. In myocardial hypertrophy, an important role is played by a newly discovered cardiotrophin-1, a member of the IL - 6 family. The activity of IL - 6 is associated with the development of abdominal aortic aneurysm (AAA); in fact, it has been shown that the concentration of IL - 6 positively correlates with AAA diameters. C-reactive protein (CRP) is one of the biomarkers of cardiovascular diseases. Local production of CRP by the smooth muscular and endothelial cells of the vessel leads to the development of atherosclerosis to a large extent. Oxidized low-density lipoprotein (ox - LDL) also has an important role in the development of atherosclerosis. After penetrating the intima of the vessel, ox - LDL induces monocyte collection, i.e. monocytes are translated into macrophages that bind ox - LDL. Having filled the macrophages with ox - LDL, the signals of cell death are activated, which leads to the creation of foamy cells that make up the initial part of the atherosclerotic plaque. New knowledge about the mechanism of action and the role of biomarkers in the development of cardiovascular diseases will certainly provide an opportunity to prevent the onset of these disorders, as well as an adequate therapy in the treatment of cardiovascular diseases, which is one of the main goals of intensive research in the field of biomarkers.
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47

Shirakawa, Kohsuke, and Motoaki Sano. "Osteopontin in Cardiovascular Diseases." Biomolecules 11, no. 7 (July 16, 2021): 1047. http://dx.doi.org/10.3390/biom11071047.

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Unprecedented advances in secondary prevention have greatly improved the prognosis of cardiovascular diseases (CVDs); however, CVDs remain a leading cause of death globally. These findings suggest the need to reconsider cardiovascular risk and optimal medical therapy. Numerous studies have shown that inflammation, pro-thrombotic factors, and gene mutations are focused not only on cardiovascular residual risk but also as the next therapeutic target for CVDs. Furthermore, recent clinical trials, such as the Canakinumab Anti-inflammatory Thrombosis Outcomes Study trial, showed the possibility of anti-inflammatory therapy for patients with CVDs. Osteopontin (OPN) is a matricellular protein that mediates diverse biological functions and is involved in a number of pathological states in CVDs. OPN has a two-faced phenotype that is dependent on the pathological state. Acute increases in OPN have protective roles, including wound healing, neovascularization, and amelioration of vascular calcification. By contrast, chronic increases in OPN predict poor prognosis of a major adverse cardiovascular event independent of conventional cardiovascular risk factors. Thus, OPN can be a therapeutic target for CVDs but is not clinically available. In this review, we discuss the role of OPN in the development of CVDs and its potential as a therapeutic target.
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48

ETO, Tanenao. "Adrenomedullin in Cardiovascular diseases." Journal of Japan Atherosclerosis Society 27, no. 3 (2000): 69–74. http://dx.doi.org/10.5551/jat1973.27.3_69.

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49

Nuralieva, N. F., and D. A. Napalkov. "Depression and Cardiovascular Diseases." Annals of the Russian academy of medical sciences 69, no. 9-10 (2014): 21–26. http://dx.doi.org/10.15690/vramn.v69i9-10.1127.

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50

Nuralieva, N. F., and D. A. Napalkov. "DEPRESSION AND CARDIOVASCULAR DISEASES." Annals of the Russian academy of medical sciences 69, no. 9-10 (October 20, 2014): 21–26. http://dx.doi.org/10.15690/vramn384.

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Depression is considered to be an independent cardiovascular risk factor and it may worsen the symptoms of already established cardiovascular pathology such as coronary heart disease, chronic heart failure, stroke and hypertension. 3 key psychobiological mechanisms by means of which depression influences cardiovascular system: disbalance in stress response of endocrine system, hyperregulation of autonomic nervous system and immune disorders leading to dysregulation of acute phase proteins and proinflammatory cytokines release. In majority of studies in patients with depression and cardiovascular diseases it was shown that antidepressants improve the symptoms. By the way, in some studies controversial results were obtained. Future studies in this direction with involvement of cardiologists and psychiatrists should be held.
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