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      Aging-Induced Biological Changes and Cardiovascular Diseases

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          Abstract

          Aging is characterized by functional decline in homeostatic regulation and vital cellular events. This process can be linked with the development of cardiovascular diseases (CVDs). In this review, we discussed aging-induced biological alterations that are associated with CVDs through the following aspects: (i) structural, biochemical, and functional modifications; (ii) autonomic nervous system (ANS) dysregulation; (iii) epigenetic alterations; and (iv) atherosclerosis and stroke development. Aging-mediated structural and biochemical modifications coupled with gradual loss of ANS regulation, vascular stiffening, and deposition of collagen and calcium often disrupt cardiovascular system homeostasis. The structural and biochemical adjustments have been consistently implicated in the progressive increase in mechanical burden and functional breakdown of the heart and vessels. In addition, cardiomyocyte loss in this process often reduces adaptive capacity and cardiovascular function. The accumulation of epigenetic changes also plays important roles in the development of CVDs. In summary, the understanding of the aging-mediated changes remains promising towards effective diagnosis, discovery of new drug targets, and development of new therapies for the treatment of CVDs.

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          Cellular senescence in aging and age-related disease: from mechanisms to therapy.

          Bennett Childs, Matej Durik, Darren J. Baker … (2015)
          Cellular senescence, a process that imposes permanent proliferative arrest on cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related disease, and it is an attractive target for therapeutic exploitation. A wealth of information about senescence in cultured cells has been acquired over the past half century; however, senescence in living organisms is poorly understood, largely because of technical limitations relating to the identification and characterization of senescent cells in tissues and organs. Furthermore, newly recognized beneficial signaling functions of senescence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-aging therapy may have negative consequences. Here we discuss current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy.
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            The intersection between aging and cardiovascular disease.

            Brian North, David A Sinclair (2012)
            The average lifespan of humans is increasing, and with it the percentage of people entering the 65 and older age group is growing rapidly and will continue to do so in the next 20 years. Within this age group, cardiovascular disease will remain the leading cause of death, and the cost associated with treatment will continue to increase. Aging is an inevitable part of life and unfortunately poses the largest risk factor for cardiovascular disease. Although numerous studies in the cardiovascular field have considered both young and aged humans, there are still many unanswered questions as to how the genetic pathways that regulate aging in model organisms influence cardiovascular aging. Likewise, in the molecular biology of aging field, few studies fully assess the role of these aging pathways in cardiovascular health. Fortunately, this gap is beginning to close, and these two fields are merging together. We provide an overview of some of the key genes involved in regulating lifespan and health span, including sirtuins, AMP-activated protein kinase, mammalian target of rapamycin, and insulin-like growth factor 1 and their roles regulating cardiovascular health. We then discuss a series of review articles that will appear in succession and provide a more comprehensive analysis of studies carried out linking genes of aging and cardiovascular health, and perspectives of future directions of these two intimately linked fields.
            Article 0 comments Cited 442 times – based on 0 reviews     Review now
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              Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial.

              Robert Bresalier, Robert Sandler, Hui Quan … (2005)
              Selective inhibition of cyclooxygenase-2 (COX-2) may be associated with an increased risk of thrombotic events, but only limited long-term data have been available for analysis. We report on the cardiovascular outcomes associated with the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, randomized, placebo-controlled, double-blind trial designed to determine the effect of three years of treatment with rofecoxib on the risk of recurrent neoplastic polyps of the large bowel in patients with a history of colorectal adenomas. A total of 2586 patients with a history of colorectal adenomas underwent randomization: 1287 were assigned to receive 25 mg of rofecoxib daily, and 1299 to receive placebo. All investigator-reported serious adverse events that represented potential thrombotic cardiovascular events were adjudicated in a blinded fashion by an external committee. A total of 46 patients in the rofecoxib group had a confirmed thrombotic event during 3059 patient-years of follow-up (1.50 events per 100 patient-years), as compared with 26 patients in the placebo group during 3327 patient-years of follow-up (0.78 event per 100 patient-years); the corresponding relative risk was 1.92 (95 percent confidence interval, 1.19 to 3.11; P=0.008). The increased relative risk became apparent after 18 months of treatment; during the first 18 months, the event rates were similar in the two groups. The results primarily reflect a greater number of myocardial infarctions and ischemic cerebrovascular events in the rofecoxib group. There was earlier separation (at approximately five months) between groups in the incidence of nonadjudicated investigator-reported congestive heart failure, pulmonary edema, or cardiac failure (hazard ratio for the comparison of the rofecoxib group with the placebo group, 4.61; 95 percent confidence interval, 1.50 to 18.83). Overall and cardiovascular mortality was similar in the two groups. Among patients with a history of colorectal adenomas, the use of rofecoxib was associated with an increased cardiovascular risk. Copyright 2005 Massachusetts Medical Society.
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                Author and article information

                Contributors
                James Oluwagbamigbe Fajemiroye:
                ORCID: http://orcid.org/0000-0001-7440-7581
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2018
                Publication date (Electronic): 10 June 2018
                Volume: 2018
                Electronic Location Identifier: 7156435
                Affiliations
                1Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil
                2Center for Studies and Toxicological-Pharmacological Research, Faculty of Pharmacy, Federal University of Goiás, Goiânia, Brazil
                3University Center of Anápolis-Unievangélica, 75083-515 Anápolis, GO, Brazil
                4Department of Basic Sciences, Universidad Santo Tomas, Campus Osorno, Osorno, Chile
                5Department of Physiology, Ben-Carson (Snr) School of Medicine, Babcock University, Nigeria
                6Department of Natural Sciences, Special Academic Unit of Human Sciences, Federal University of Goiás, Goiânia, Goiás, Brazil
                7Laboratory of Experimental Physiology, Faculty of Physical Education, Federal University of Uberlândia, Uberlândia, Minas Gerais, Brazil
                Author notes

                Academic Editor: Jun Ren

                Author information
                http://orcid.org/0000-0001-7440-7581
                http://orcid.org/0000-0002-4749-869X
                http://orcid.org/0000-0003-3516-5350
                http://orcid.org/0000-0003-0488-5400
                Article
                DOI: 10.1155/2018/7156435
                PMC ID: 6015721
                PubMed ID: 29984246
                SO-VID: 418a9d79-61a2-45fd-a60d-91fc964ec065
                Copyright © Copyright © 2018 James Oluwagbamigbe Fajemiroye et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 21 December 2017
                Date revision received : 23 April 2018
                Date accepted : 3 May 2018
                Funding
                Funded by: Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
                Funded by: Conselho Nacional de Desenvolvimento Científico e Tecnológico
                Funded by: Fundação de Amparo à Pesquisa do Estado de Goiás
                Categories
                Subject: Review Article

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