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- W3092444587 endingPage "111380" @default.
- W3092444587 startingPage "111380" @default.
- W3092444587 abstract "Severity of cardiovascular disease increases markedly in elderly patients. In addition, many therapeutic strategies that decrease cardiac injury in adult patients are invalid in elderly patients. Thus, it is a challenge to protect the aged heart in the context of underlying chronic or acute cardiac diseases including ischemia-reperfusion injury. The cause(s) of this age-related increased damage remain unknown. Aging impairs the function of the mitochondrial electron transport chain (ETC), leading to decreased energy production and increased oxidative stress due to generation of reactive oxygen species (ROS). Additionally, ROS-induced oxidative stress can increase cardiac injury during ischemia-reperfusion by potentiating mitochondrial permeability transition pore (MPTP) opening. Aging leads to increased endoplasmic reticulum (ER) stress, which contributes to mitochondrial dysfunction, including reduced function of the ETC. The activation of both cytosolic and mitochondrial calcium-activated proteases termed calpains leads to mitochondrial dysfunction and decreased ETC function. Intriguingly, mitochondrial ROS generation also induces ER stress, highlighting the dynamic interaction between mitochondria and ER. Here, we discuss the role of ER stress in sensitizing and potentiating mitochondrial dysfunction in response to ischemia-reperfusion, and the promising potential therapeutic benefit of inhibition of ER stress and / or calpains to attenuate cardiac injury in elderly patients." @default.
- W3092444587 created "2020-10-15" @default.
- W3092444587 creator A5012571820 @default.
- W3092444587 creator A5012917190 @default.
- W3092444587 creator A5072315648 @default.
- W3092444587 date "2020-12-01" @default.
- W3092444587 modified "2023-09-29" @default.
- W3092444587 title "Targeting ER stress and calpain activation to reverse age-dependent mitochondrial damage in the heart" @default.
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