Exercise Attenuates Myocardial Ischemia-Reperfusion Injury by Regulating Endoplasmic Reticulum Stress and Mitophagy Through M<sub>2</sub> Acetylcholine Receptor

Chen, Wei; Ma, Mei; Song, Yinping; Hua, Yijie; Jia, Hao; Liu, Jiankang; Wang, Youhua

doi:10.1089/ars.2022.0168

Cited by 11 publications

(3 citation statements)

References 35 publications

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“…The permanent ligation of the left anterior descending coronary artery (LAD) in Parkin-deficient mice leads to increased mortality, and the surviving animals are characterized by impaired heart function and decreased mitophagy [246]. Mitophagy is initiated by myocardial I/R injury in rat hearts in vivo, as indicated by the increased expression of PINK1 and Parkin [247][248][249][250]. The amounts of PINK1 are also induced in the mitochondria of H9C2 cells subjected to hypoxia/reoxygenation [250] and upon permanent LAD ligation in mice [251].…”

Section: Pten-induced Putative Kinase 1 (Pink1)mentioning

confidence: 99%

Mitochondrial Kinase Signaling for Cardioprotection

Boengler,

Eickelmann,

Kleinbongard

2024

IJMS

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Myocardial ischemia/reperfusion injury is reduced by cardioprotective adaptations such as local or remote ischemic conditioning. The cardioprotective stimuli activate signaling cascades, which converge on mitochondria and maintain the function of the organelles, which is critical for cell survival. The signaling cascades include not only extracellular molecules that activate sarcolemmal receptor-dependent or -independent protein kinases that signal at the plasma membrane or in the cytosol, but also involve kinases, which are located to or within mitochondria, phosphorylate mitochondrial target proteins, and thereby modify, e.g., respiration, the generation of reactive oxygen species, calcium handling, mitochondrial dynamics, mitophagy, or apoptosis. In the present review, we give a personal and opinionated overview of selected protein kinases, localized to/within myocardial mitochondria, and summarize the available data on their role in myocardial ischemia/reperfusion injury and protection from it. We highlight the regulation of mitochondrial function by these mitochondrial protein kinases.

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Section: Pten-induced Putative Kinase 1 (Pink1)mentioning

confidence: 99%

Mitochondrial Kinase Signaling for Cardioprotection

Boengler,

Eickelmann,

Kleinbongard

2024

IJMS

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“…Cardiomyocytes express high levels of endoplasmic reticulum stress-related signaling proteins, including transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), glucose regulatory protein 78 (GRP78), etc. Treatments that Inhibit the signaling of endoplasmic reticulum stress can effectively reduce the rate of cell death in conditions like myocardial ischemiareperfusion injury (61)(62)(63)(64). Key cellular events in the pathogenesis of MIRI are summarized in Figure 1.…”

Section: Endoplasmic Reticulum Stressmentioning

confidence: 99%

Salvianolic acids and its potential for cardio-protection against myocardial ischemic reperfusion injury in diabetes

Jiang,

Cai,

Han

et al. 2024

Front. Endocrinol.

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The incidence of diabetes and related mortality rate increase yearly in modern cities. Additionally, elevated glucose levels can result in an increase of reactive oxygen species (ROS), ferroptosis, and the disruption of protective pathways in the heart. These factors collectively heighten the vulnerability of diabetic individuals to myocardial ischemia. Reperfusion therapies have been effectively used in clinical practice. There are limitations to the current clinical methods used to treat myocardial ischemia-reperfusion injury. As a result, reducing post-treatment ischemia/reperfusion injury remains a challenge. Therefore, efforts are underway to provide more efficient therapy. Salvia miltiorrhiza Bunge (Danshen) has been used for centuries in ancient China to treat cardiovascular diseases (CVD) with rare side effects. Salvianolic acid is a water-soluble phenolic compound with potent antioxidant properties and has the greatest hydrophilic property in Danshen. It has recently been discovered that salvianolic acids A (SAA) and B (SAB) are capable of inhibiting apoptosis by targeting the JNK/Akt pathway and the NF-κB pathway, respectively. This review delves into the most recent discoveries regarding the therapeutic and cardioprotective benefits of salvianolic acid for individuals with diabetes. Salvianolic acid shows great potential in myocardial protection in diabetes mellitus. A thorough understanding of the protective mechanism of salvianolic acid could expand its potential uses in developing medicines for treating diabetes mellitus related myocardial ischemia-reperfusion.

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“…Notch1 suppresses the PTEN-PINK1-Parkin signaling and downregulates mitochondrial fusion/fission and mitochondrial autophagy, conferring protection against I/R injury in cardiomyocytes and a rat I/R injury model [ 203 ]. In I/R rat models, exercise-induced parasympathetic nerve function increased myocardial M2 acetylcholine receptor (M 2 AChR) protein expression and effectively reduced mitophagy, endoplasmic reticulum stress (ERS), and apoptosis [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Mitophagy for cardioprotection

Titus,

Sung,

Zablocki

et al. 2023

Basic Res Cardiol

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Mitochondrial function is maintained by several strictly coordinated mechanisms, collectively termed mitochondrial quality control mechanisms, including fusion and fission, degradation, and biogenesis. As the primary source of energy in cardiomyocytes, mitochondria are the central organelle for maintaining cardiac function. Since adult cardiomyocytes in humans rarely divide, the number of dysfunctional mitochondria cannot easily be diluted through cell division. Thus, efficient degradation of dysfunctional mitochondria is crucial to maintaining cellular function. Mitophagy, a mitochondria specific form of autophagy, is a major mechanism by which damaged or unnecessary mitochondria are targeted and eliminated. Mitophagy is active in cardiomyocytes at baseline and in response to stress, and plays an essential role in maintaining the quality of mitochondria in cardiomyocytes. Mitophagy is mediated through multiple mechanisms in the heart, and each of these mechanisms can partially compensate for the loss of another mechanism. However, insufficient levels of mitophagy eventually lead to mitochondrial dysfunction and the development of heart failure. In this review, we discuss the molecular mechanisms of mitophagy in the heart and the role of mitophagy in cardiac pathophysiology, with the focus on recent findings in the field.

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Exercise Attenuates Myocardial Ischemia-Reperfusion Injury by Regulating Endoplasmic Reticulum Stress and Mitophagy Through M₂ Acetylcholine Receptor

Cited by 11 publications

References 35 publications

Mitochondrial Kinase Signaling for Cardioprotection

Mitochondrial Kinase Signaling for Cardioprotection

Salvianolic acids and its potential for cardio-protection against myocardial ischemic reperfusion injury in diabetes

Mitophagy for cardioprotection

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Exercise Attenuates Myocardial Ischemia-Reperfusion Injury by Regulating Endoplasmic Reticulum Stress and Mitophagy Through M2 Acetylcholine Receptor

Cited by 11 publications

References 35 publications

Mitochondrial Kinase Signaling for Cardioprotection

Mitochondrial Kinase Signaling for Cardioprotection

Salvianolic acids and its potential for cardio-protection against myocardial ischemic reperfusion injury in diabetes

Mitophagy for cardioprotection

Contact Info

Product

Resources

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Exercise Attenuates Myocardial Ischemia-Reperfusion Injury by Regulating Endoplasmic Reticulum Stress and Mitophagy Through M₂ Acetylcholine Receptor