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Tepp 2017 Mol Cell Biochem

From Bioblast
Publications in the MiPMap
Tepp K, Puurand M, Timohhina N, Adamson J, Klepinin A, Truu L, Shevchuk I, Chekulayev V, Kaambre T (2017) Changes in the mitochondrial function and in the efficiency of energy transfer pathways during cardiomyocyte aging. Mol Cell Biochem 432:141-58.

Β» PMID: 28293876

Tepp K, Puurand M, Timohhina N, Adamson J, Klepinin A, Truu L, Shevchuk I, Chekulayev V, Kaambre T (2017) Mol Cell Biochem

Abstract: The role of mitochondria in alterations that take place in the muscle cell during healthy aging is a matter of debate during recent years. Most of the studies in bioenergetics have a focus on the model of isolated mitochondria, while changes in the crosstalk between working myofibrils and mitochondria in senescent cardiomyocytes have been less studied. The aim of our research was to investigate the modifications in the highly regulated ATP production and energy transfer systems in heart cells in old rat cardiomyocytes. The results of our work demonstrated alterations in the diffusion restrictions of energy metabolites, manifested by changes in the apparent Michaelis-Menten constant of mitochondria to exogenous ADP. The creatine kinase (CK) phosphotransfer pathway efficiency declines significantly in senescence. The ability of creatine to stimulate OXPHOS as well as to increase the affinity of mitochondria for ADP is falling and the most critical decline is already in the 1-year group (middle-age model in rats). Also, a moderate decrease in the adenylate kinase phosphotransfer system was detected. The importance of glycolysis increases in senescence, while the hexokinase activity does not change during healthy aging. The main result of our study is that the decline in the heart muscle performance is not caused by the changes in the respiratory chain complexes activity but mainly by the decrease in the energy transfer efficiency, especially by the CK pathway. β€’ Keywords: Adenylate kinase, Aging, Cardiomyocytes, Creatine kinase, Energy metabolism, Mitochondria β€’ Bioblast editor: Kandolf G β€’ O2k-Network Lab: EE Tallinn Kaambre T, EE Tallinn Saks VA

Labels: MiParea: Respiration  Pathology: Aging;senescence 

Organism: Rat  Tissue;cell: Heart  Preparation: Permeabilized cells 

Regulation: ADP, ATP production  Coupling state: LEAK, OXPHOS  Pathway: N, S, CIV, ROX  HRR: Oxygraph-2k