Regulatory mechanisms of mitochondrial function and cardiac aging
|Author:||Lin, Ruizhu1,2; Kerkelä, Risto1,2,3|
1Research Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, FI-90014 Oulu, Finland
2Medical Research Centre Oulu, Oulu University Hospital and University of Oulu, FI-90014 Oulu, Finland
3Biocenter Oulu, University of Oulu, FI-90014 Oulu, Finland
|Online Access:||PDF Full Text (PDF, 0.7 MB)|
|Persistent link:|| http://urn.fi/urn:nbn:fi-fe2020041618867
Multidisciplinary Digital Publishing Institute,
|Publish Date:|| 2020-04-16
Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult. Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Aging and cardiac pathologies are also associated with increased senescence in the heart. However, the cause and consequences of cardiac senescence during aging or in cardiac pathologies are mostly unrecognized. Further, despite recent advancement in anti-senescence therapy, the targeted cell type and the effect on cardiac structure and function have been largely overlooked. The unique cellular composition of the heart, and especially the functional properties of cardiomyocytes, need to be considered when designing therapeutics to target cardiac aging. Here we review recent findings regarding key factors regulating cell senescence, mitochondrial health as well as cardiomyocyte rejuvenation.
International journal of molecular sciences
|Type of Publication:||
A1 Journal article – refereed
|Field of Science:||
This work was supported by grants from the Academy of Finland (grant No.: 297094 to R.K.), Jane and Aatos Erkko Foundation and the Finnish Foundation for Cardiovascular Research.
|Academy of Finland Grant Number:||
297094 (Academy of Finland Funding decision)
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).