The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
The role of sirtuins in cardiac disease
Open accessAbstract
Modification of histones is one of the important mechanisms of epigenetics, in which genetic control is determined by factors other than an individual's DNA sequence. Sirtuin family proteins, which are class III histone deacetylases, were originally identified as gene silencers that affect the mating type of yeast, leading to the name “silent mating-type information regulation 2” (SIR2). They are characterized by their requirement of nicotinamide adenine dinucleotide for their enzyme activity, unlike other classes of histone deacetylases. Sirtuins have been traditionally linked to longevity and the beneficial effects of calorie restriction and DNA damage repair. Recently, sirtuins have been shown to be involved in a wide range of physiological and pathological processes, including aging, energy responses to low calorie availability, and stress resistance, as well as apoptosis and inflammation. Sirtuins can also regulate mitochondrial biogenesis and circadian clocks. Seven sirtuin family proteins (Sirt1-7) have been identified as mammalian SIR2 orthologs, localized in different subcellular compartments, namely, the cytoplasm (Sirt1, 2), the mitochondria (Sirt3, 4, 5), and the nucleus (Sirt1, 2, 6, 7). Sirt1 is evolutionarily close to yeast SIR2 and has been the most intensively investigated in the cardiovascular system. Endogenous Sirt1 plays a pivotal role in mediating the cell death/survival process and has been implicated in the pathogenesis of cardiovascular disease. Downregulation of Sirt2 is protective against ischemic-reperfusion injury. Increased Sirt3 expression has been shown to correlate with longevity in humans. In addition, Sirt3 protects cardiomyocytes from aging and oxidative stress and suppresses cardiac hypertrophy. Sirt6 has also recently been demonstrated to attenuate cardiac hypertrophy, and Sirt7 is known to regulate apoptosis and stress responses in the heart. On the other hand, the roles of Sirt4 and Sirt5 in the heart remain largely uncharacterized.
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1 retracted
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The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system
Kietzmann, T., Petry, A., Shvetsova, A., Gerhold, J. M., & Görlach, A. (2017) · British Journal of Pharmacology · doi:10.1111/bph.13792 · Cited by 253
Zhao, L., Tao, X., Qi, Y., Xu, L., Yin, L., & Peng, J. (2018) · Redox Biology · doi:10.1016/j.redox.2018.02.026 · Cited by 202
CD38 promotes angiotensin II‐induced cardiac hypertrophy
Guan, X., Hong, X., Zhao, N., Liu, X., Xiao, Y., Chen, T., Deng, L., Wang, X., Wang, J., Ji, G., et al. (2017) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13076 · Cited by 90
Obesity accelerates cardiovascular ageing
Ruperez, C., Madeo, F., de Cabo, R., Kroemer, G., & Abdellatif, M. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf216 · Cited by 73
Ruiz-Meana, M., Bou-Teen, D., Ferdinandy, P., Gyongyosi, M., Pesce, M., Perrino, C., Schulz, R., Sluijter, J. P. G., Tocchetti, C. G., Thum, T., et al. (2020) · Cardiovascular Research · doi:10.1093/cvr/cvaa132 · Cited by 67
Sirtuins at the Service of Healthy Longevity
Watroba, M., & Szukiewicz, D. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.724506 · Cited by 64
Could sirtuin activities modify ALS onset and progression?
Tang, B. L. (2017) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-016-0452-2 · Cited by 24
Metadata
- Authors
- Matsushima, S., & Sadoshima, J.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2015-11
- Volume
- 309
- Issue
- 9
- Pages
- H1375-H1389
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2142270756
- Cited by
- 375
- References
- 28
- FWCI
- 13.99
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
