运动训练可通过 DRP1 减少缺血再灌注心脏中的线粒体碎片。

IF 3.3 2区医学 Q1 PHYSIOLOGY

Journal of General Physiology Pub Date : 2024-12-02 Epub Date: 2024-11-07 DOI:10.1085/jgp.202313485

Mathilde Dubois, Florian Pallot, Maxime Gouin-Gravezat, Doria Boulghobra, Florence Coste, Guillaume Walther, Gregory Meyer, Isabelle Bornard, Cyril Reboul

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引用次数: 0

摘要

线粒体分裂是心脏缺血再灌注损伤（IR）的关键诱因。运动训练是一种有效的心脏保护策略，但它对红外损伤期间线粒体分裂的影响仍然未知。通过使用离体大鼠心脏，我们发现运动训练限制了动态样蛋白 1 的激活，并限制了线粒体在 IR 期间的破碎。这些结果支持了运动训练通过调节红外过程中线粒体破碎的能力来促进心脏保护的假设。

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Exercise training may reduce fragmented mitochondria in the ischemic-reperfused heart through DRP1.

Mitochondrial fission is a key trigger of cardiac ischemia-reperfusion injuries (IR). Exercise training is an efficient cardioprotective strategy, but its impact on mitochondrial fragmentation during IR remains unknown. Using isolated rat hearts, we found that exercise training limited the activation of dynamin-like protein 1 and limited mitochondrial fragmentation during IR. These results support the hypothesis that exercise training contributes to cardioprotection through its capacity to modulate the mitochondrial fragmentation during IR.

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来源期刊

Journal of General Physiology 医学-生理学

CiteScore

6.00

自引率

10.50%

发文量

审稿时长

6-12 weeks

期刊介绍： General physiology is the study of biological mechanisms through analytical investigations, which decipher the molecular and cellular mechanisms underlying biological function at all levels of organization. The mission of Journal of General Physiology (JGP) is to publish mechanistic and quantitative molecular and cellular physiology of the highest quality, to provide a best-in-class author experience, and to nurture future generations of independent researchers. The major emphasis is on physiological problems at the cellular and molecular level.