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The primary role of an adult cardiomyocytes is to contract rhythmically to allow the production of force and the propulsion of blood, they are required to react rapidly to environmental stimuli and they act as a sophisticated support system for the myofilaments which conduct cellular contraction. The contraction of this protein system is defined by the cyclic modulation of calcium concentrations (1). Cardiomyocytes contraction is triggered by an electrical stimulus, the action potential (AP), which induces transient depolarization of the cardiomyocyte plasma membrane (the sarcolemma) (2).
cardiomyocytes and Excitation–contraction coupling (ECC) process

  Excitation–contraction coupling (ECC). (1) An action potential depolarizes the cardiomyocyte and induces Na+ influx through voltage-gated Na+ channels (Nav). (2) This further depolarizes the cell membrane and induces Ca2+ influx through voltage-gated L-type Ca2+ channels (LTCCs). (3) This Ca2+ entry stimulates Ca2+ release via dyadic RyR2 on the SR (4), which in turn triggers cell contraction through activating myofilament crossbridges. (5) LTCC inactivate and RyR close. (6) Cytosolic Ca2+ is then moved out of the cell by the Na+/Ca2+ exchanger (NCX) and pumped back into the SR by SERCA2a, thereby decreasing cytosolic Ca2+ concentration and bringing about relaxation. (7) A family of K+ channels participate in cell repolarization with K+ efflux as a last step for returning membrane potential to its resting value before a new cycle starts. (8) Tuning ECC to meet cardiovascular demands involves β-adrenergic pathways that induce the activation of CaMKII and of cAMP/PKA, which phosphorylates voltage-gated LTCCs and RyRs to enhance their activity and phospholamban (PLB) to remove its inhibition of SERCA activity (2) .


Cell death in the heart is detrimental because the majority of adult cardiomyocytes are terminally differentiated and non-regenerative cells with a limited capacity to perform key functions (3). Cardiac diseases, characterized by cardiomyocyte loss, lead to dramatic impairment of cardiac function and ultimately to congestive heart failure (4). Upon infarction, the remaining cardiomyocytes cannot undergo hyperplasia. Instead, the remaining cardiomyocytes can increase protein synthesis, cell size, the number of sarcomeres, the number of contractile proteins, and the number of mitochondria (5).

(1) Judina A, Gorelik J, Wright PT. Studying signal compartmentation in adult cardiomyocytes. Biochem Soc Trans. (2020);48(1):61-70.
(2) Gilbert G, et al. Calcium Signaling in Cardiomyocyte Function. Cold Spring Harb Perspect Biol. (2020);12(3):a035428.
(3) Zhang G, et al. Cardiomyocyte death in sepsis: Mechanisms and regulation (Review). Mol Med Rep. (2022);26(2):257.
(4) Duong MN et al. The fat and the bad: Mature adipocytes, key actors in tumor progression and resistance. Oncotarget. (2017).
(5) Choi J et al. Adipocyte biology in breast cancer: From silent bystander to active facilitator. Prog Lipid Res. (2018);(69):11-20.


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