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Difference between revisions of "Xu 2022 Sci Adv"

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{{Publication
{{Publication
|title=Xu H, Ahn B, Van Remmen H (2022) Impact of aging and oxidative stress on specific components of excitation contraction coupling in regulating force generation.
|title=Xu H, Ahn B, Van Remmen H (2022) Impact of aging and oxidative stress on specific components of excitation contraction coupling in regulating force generation. https://doi.org/10.1126/sciadv.add7377
|info=Sci Adv 8:eadd7377. [https://www.ncbi.nlm.nih.gov/pubmed/36288318 PMID: 36288318 Open Access]
|info=Sci Adv 8:eadd7377. [https://www.ncbi.nlm.nih.gov/pubmed/36288318 PMID: 36288318 Open Access]
|authors=Xu H, Ahn B, Van Remmen H
|authors=Xu H, Ahn B, Van Remmen H
|year=2022
|year=2022
|journal=Sci Adv
|journal=Sci Adv
|abstract=Muscle weakness associated with sarcopenia is a major contributor to reduced health span and quality of life in the elderly. However, the underlying mechanisms of muscle weakness in aging are not fully defined. We investigated the effect of oxidative stress and aging on specific molecular mechanisms involved in muscle force production in mice and skinned permeabilized single fibers in mice lacking the antioxidant enzyme CuZnSod (Sod1KO) and in aging (24-month-old) wild-type mice. Loss of muscle strength occurs in both models, potentially because of reduced membrane excitability with altered NKA signaling and RyR stability, decreased fiber Ca2+ sensitivity and suppressed SERCA activity via modification of the Cys674 residue, dysregulated SR and cytosolic Ca2+ homeostasis, and impaired mitochondrial Ca2+ buffering and respiration. Our results provide a better understanding of the specific impacts of aging and oxidative stress on mechanisms related to muscle weakness that may point to future interventions for countering muscle weakness.
|abstract=Muscle weakness associated with sarcopenia is a major contributor to reduced health span and quality of life in the elderly. However, the underlying mechanisms of muscle weakness in aging are not fully defined. We investigated the effect of oxidative stress and aging on specific molecular mechanisms involved in muscle force production in mice and skinned permeabilized single fibers in mice lacking the antioxidant enzyme CuZnSod (Sod1KO) and in aging (24-month-old) wild-type mice. Loss of muscle strength occurs in both models, potentially because of reduced membrane excitability with altered NKA signaling and RyR stability, decreased fiber Ca<sup>2+</sup> sensitivity and suppressed SERCA activity via modification of the Cys<sup>674</sup> residue, dysregulated SR and cytosolic Ca<sup>2+</sup> homeostasis, and impaired mitochondrial Ca<sup>2+</sup> buffering and respiration. Our results provide a better understanding of the specific impacts of aging and oxidative stress on mechanisms related to muscle weakness that may point to future interventions for countering muscle weakness.
|editor=[[Plangger M]]
|editor=[[Plangger M]]
}}
}}

Revision as of 13:49, 2 November 2022

Publications in the MiPMap
Xu H, Ahn B, Van Remmen H (2022) Impact of aging and oxidative stress on specific components of excitation contraction coupling in regulating force generation. https://doi.org/10.1126/sciadv.add7377

Β» Sci Adv 8:eadd7377. PMID: 36288318 Open Access

Xu H, Ahn B, Van Remmen H (2022) Sci Adv

Abstract: Muscle weakness associated with sarcopenia is a major contributor to reduced health span and quality of life in the elderly. However, the underlying mechanisms of muscle weakness in aging are not fully defined. We investigated the effect of oxidative stress and aging on specific molecular mechanisms involved in muscle force production in mice and skinned permeabilized single fibers in mice lacking the antioxidant enzyme CuZnSod (Sod1KO) and in aging (24-month-old) wild-type mice. Loss of muscle strength occurs in both models, potentially because of reduced membrane excitability with altered NKA signaling and RyR stability, decreased fiber Ca2+ sensitivity and suppressed SERCA activity via modification of the Cys674 residue, dysregulated SR and cytosolic Ca2+ homeostasis, and impaired mitochondrial Ca2+ buffering and respiration. Our results provide a better understanding of the specific impacts of aging and oxidative stress on mechanisms related to muscle weakness that may point to future interventions for countering muscle weakness.

β€’ Bioblast editor: Plangger M


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2022-11