scholarly journals The Role of Mitochondrial Quality Control in Cardiac Ischemia/Reperfusion Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jia Huang ◽  
Ruibing Li ◽  
Chengbin Wang
Keyword(s):  
Quality Control ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Mitochondrial Morphology ◽  
Mitochondrial Network ◽  
Mitochondrial Quality Control

A healthy mitochondrial network produces a large amount of ATP and biosynthetic intermediates to provide sufficient energy for myocardium and maintain normal cell metabolism. Mitochondria form a dynamic and interconnected network involved in various cellular metabolic signaling pathways. As mitochondria are damaged, controlling mitochondrial quantity and quality is activated by changing their morphology and tube network structure, mitophagy, and biogenesis to replenish a healthy mitochondrial network to preserve cell function. There is no doubt that mitochondrial dysfunction has become a key factor in many diseases. Ischemia/reperfusion (IR) injury is a pathological manifestation of various heart diseases. Cardiac ischemia causes temporary tissue and organelle damage. Although reperfusion is essential to compensate for nutrient deficiency, blood flow restoration inconsequently further kills the previously ischemic cardiomyocytes. To date, dysfunctional mitochondria and disturbed mitochondrial quality control have been identified as critical IR injury mechanisms. Many researchers have detected abnormal mitochondrial morphology and mitophagy, as well as aberrant levels and activity of mitochondrial biogenesis factors in the IR injury model. Although mitochondrial damage is well-known in myocardial IR injury, the causal relationship between abnormal mitochondrial quality control and IR injury has not been established. This review briefly describes the molecular mechanisms of mitochondrial quality control, summarizes our current understanding of the complex role of mitochondrial quality control in IR injury, and finally speculates on the possibility of targeted control of mitochondria and the methods available to mitigate IR injury.

scholarly journals Role of GTPase-Dependent Mitochondrial Dynamins in Heart Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Jiangen Liu ◽  
Xianjing Song ◽  
Youyou Yan ◽  
Bin Liu
Keyword(s):  
Cell Function ◽  
Morphological Changes ◽  
Heart Function ◽  
Mitochondrial Dynamics ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Mitochondrial Fusion ◽  
Dependent Manner

Heart function maintenance requires a large amount of energy, which is supplied by the mitochondria. In addition to providing energy to cardiomyocytes, mitochondria also play an important role in maintaining cell function and homeostasis. Although adult cardiomyocyte mitochondria appear as independent, low-static organelles, morphological changes have been observed in cardiomyocyte mitochondria under stress or pathological conditions. Indeed, cardiac mitochondrial fission and fusion are involved in the occurrence and development of heart diseases. As mitochondrial fission and fusion are primarily regulated by mitochondrial dynamins in a GTPase-dependent manner, GTPase-dependent mitochondrial fusion (MFN1, MFN2, and OPA1) and fission (DRP1) proteins, which are abundant in the adult heart, can also be regulated in heart diseases. In fact, these dynamic proteins have been shown to play important roles in specific diseases, including ischemia-reperfusion injury, heart failure, and metabolic cardiomyopathy. This article reviews the role of GTPase-dependent mitochondrial fusion and fission protein-mediated mitochondrial dynamics in the occurrence and development of heart diseases.

scholarly journals Molecular Mechanisms of Cardioprotective Actions of Tanshinones

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Hyou-Ju Jin ◽  
Chun-Guang Li
Keyword(s):  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Heart Diseases ◽  
Salvia Miltiorrhiza ◽  
Ischemia Reperfusion ◽  
Therapeutic Agents ◽  
Cardiac Ischemia ◽  
Mitochondrial Apoptosis ◽  
Lipophilic Compounds ◽  
Coronary Heart Diseases

Tanshinones are lipophilic compounds derived fromSalvia miltiorrhiza(Danshen) that has been widely used to treat coronary heart diseases in China. The cardioprotective actions of tanshinones have been extensively studied in various models of myocardial infarction, cardiac ischemia reperfusion injury, cardiac hypertrophy, atherosclerosis, hypoxia, and cardiomyopathy. This review outlines the recent development in understanding the molecular mechanisms and signaling pathways involved in the cardioprotective actions of tanshinones, in particular on mitochondrial apoptosis, calcium, nitric oxide, ROS, TNF-α, PKC, PI3K/Akt, IKK/NF-κB, and TGF-β1/Smad mechanisms, which highlights the potential of these compounds as therapeutic agents for treating cardiovascular diseases.

scholarly journals Mitochondrial quality control in intervertebral disc degeneration

2021 ◽  
Author(s):  
Yu Song ◽  
Saideng Lu ◽  
Wen Geng ◽  
Xiaobo Feng ◽  
Rongjin Luo ◽  
...  
Keyword(s):  
Quality Control ◽  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Current Knowledge ◽  
Mitochondrial Dynamics ◽  
Intervertebral Discs ◽  
Mitochondrial Quality Control

AbstractIntervertebral disc degeneration (IDD) is a common and early-onset pathogenesis in the human lifespan that can increase the risk of low back pain. More clarification of the molecular mechanisms associated with the onset and progression of IDD is likely to help establish novel preventive and therapeutic strategies. Recently, mitochondria have been increasingly recognized as participants in regulating glycolytic metabolism, which has historically been regarded as the main metabolic pathway in intervertebral discs due to their avascular properties. Indeed, mitochondrial structural and functional disruption has been observed in degenerated nucleus pulposus (NP) cells and intervertebral discs. Multilevel and well-orchestrated strategies, namely, mitochondrial quality control (MQC), are involved in the maintenance of mitochondrial integrity, mitochondrial proteostasis, the mitochondrial antioxidant system, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis. Here, we address the key evidence and current knowledge of the role of mitochondrial function in the IDD process and consider how MQC strategies contribute to the protective and detrimental properties of mitochondria in NP cell function. The relevant potential therapeutic treatments targeting MQC for IDD intervention are also summarized. Further clarification of the functional and synergistic mechanisms among MQC mechanisms may provide useful clues for use in developing novel IDD treatments.

scholarly journals The Role of SIRT3 in Mediating Cardioprotective Effects of RAS Inhibition on Cardiac Ischemia-Reperfusion

2015 ◽  
Vol 18 (3) ◽  
pp. 547 ◽  
Author(s):  
Sabzali Javadov ◽  
Nelson Escobales
Keyword(s):  
Angiotensin Ii ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Renin Angiotensin System ◽  
Cardiac Ischemia ◽  
Pharmaceutical Sciences ◽  
Ras Inhibition ◽  
Cardioprotective Effects

Cardiac ischemia-reperfusion stimulates the renin-angiotensin system (RAS) associated with elevated levels of circulating angiotensin II. Numerous studies demonstrate that the antagonist for the angiotensin II type 1 receptor, losartan improves cardiac function in animal models of ischemia-reperfusion. Molecular mechanisms of the cardioprotective effects of RAS inhibitors on cardiac ischemia-reperfusion remain poorly understood, and are not associated with the anti-hypertensive action of these drugs. This Commentary focuses on the study published in the Journal of Pharmacy and Pharmaceutical Sciences, 2015, 18:112-123, that elucidates the role of SIRT3 in the cardioprotective action of losartan against ischemic-reperfusion injury. We provide comprehensive discussion of the role of mitochondria in the cardioprotective effects of losartan through SIRT3. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

scholarly journals Mitophagy in Yeast: Decades of Research

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3541
Author(s):  
Bhatia-Kissova Ingrid ◽  
Camougrand Nadine
Keyword(s):  
Quality Control ◽  
Molecular Mechanisms ◽  
Mitochondrial Quality Control ◽  
Cellular Homeostasis ◽  
Selective Degradation ◽  
Proper Functioning ◽  
Unicellular Organisms ◽  
Shed Light

Mitophagy, the selective degradation of mitochondria by autophagy, is one of the most important mechanisms of mitochondrial quality control, and its proper functioning is essential for cellular homeostasis. In this review, we describe the most important milestones achieved during almost 2 decades of research on yeasts, which shed light on the molecular mechanisms, regulation, and role of the Atg32 receptor in this process. We analyze the role of ROS in mitophagy and discuss the physiological roles of mitophagy in unicellular organisms, such as yeast; these roles are very different from those in mammals. Additionally, we discuss some of the different tools available for studying mitophagy.

scholarly journals Role of Higenamine in Heart Diseases: A Mini-Review

2022 ◽  
Vol 12 ◽  
Author(s):  
Jianxia Wen ◽  
Mingjie Li ◽  
Wenwen Zhang ◽  
Haoyu Wang ◽  
Yan Bai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Disease ◽  
Reperfusion Injury ◽  
Cardiac Fibrosis ◽  
Ischemia Reperfusion Injury ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia

Higenamine, a natural product with multiple targets in heart diseases, is originally derived from Aconitum, which has been traditionally used in China for the treatment of heart disease, including heart failure, arrhythmia, bradycardia, cardiac ischemia/reperfusion injury, cardiac fibrosis, etc. This study is aimed to clarify the role of higenamine in heart diseases. Higenamine has effects on improving energy metabolism of cardiomyocytes, anti-cardiac fibroblast activation, anti-oxidative stress and anti-apoptosis. Accumulating evidence from various studies has shown that higenamine exerts a wide range of cardiovascular pharmacological effects in vivo and in vitro, including alleviating heart failure, reducing cardiac ischemia/reperfusion injury, attenuating pathological cardiac fibrosis and dysfunction. In addition, several clinical studies have reported that higenamine could continuously increase the heart rate levels of healthy volunteers as well as patients with heart disease, but there are variable effects on systolic blood pressure and diastolic blood pressure. Moreover, the heart protection and therapeutic effects of higenamine on heart disease are related to regulating LKB1/AMPKα/Sirt1, mediating the β2-AR/PI3K/AKT cascade, induction of heme oxygenase-1, suppressing TGF-β1/Smad signaling, and targeting ASK1/MAPK (ERK, P38)/NF-kB signaling pathway. However, the interventional effects of higenamine on heart disease and its underlying mechanisms based on experimental studies have not yet been systematically reviewed. This paper reviewed the potential pharmacological mechanisms of higenamine on the prevention, treatment, and diagnosis of heart disease and clarified its clinical applications. The literature shows that higenamine may have a potent effect on complex heart diseases, and proves the profound medicinal value of higenamine in heart disease.

scholarly journals Mitophagy Eliminates the Accumulation of SARM1 on the Mitochondria, Alleviating Programmed Axon Death in Acrylamide Neuropathy

2022 ◽  
Author(s):  
Shuai Wang ◽  
Hui Yong ◽  
Cuiqin Zhang ◽  
Kang Kang ◽  
Mingxue Song ◽  
...  
Keyword(s):  
Quality Control ◽  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Biological Significance ◽  
Control Mechanisms ◽  
Dependent Manner ◽  
Mitochondrial Network ◽  
Mitochondrial Localization ◽  
Mitochondrial Quality Control ◽  
Axon Loss

Abstract Sterile-α and toll/interleukin 1 receptor motif containing protein 1 (SARM1) is the central executioner of programmed axon death (Wallerian degeneration). Although it has been confirmed to have a mitochondrial targeting sequence and can bind to and stabilize PINK1 on mitochondria, the biological significance for mitochondrial localization of SARM1 is still unclear. The relationship between mitochondrial quality control mechanisms and programmed axon death also needs to be clarified. Chronic acrylamide (ACR) intoxication cause typical pathology of axon degeneration involving early axon loss. Here, we demonstrated that the SARM1 dependent Wallerian axon self-destruction pathway was activated following ACR intoxication. Moreover, increased SARM1 was observed on the mitochondria, which interfered with the mitochondrial quality control mechanisms. As a protective response to stress, mitochondrial components enriched in SARM1 were isolated from the mitochondrial network through an increased fission process and were degraded in an autophagy-dependent manner. Importantly, rapamycin (RAPA) administration eliminated mitochondrial accumulated SARM1 and inhibited axon loss. Thus, mitochondrial localization of SARM1 may be complement to the coordinated activity of NMNAT2 and SARM1, and may be part of the self-limiting molecular mechanisms of programmed axon death. In the early latent period, the mitochondrial localization of SARM1 will help it to be isolated by the mitochondrial network and to be degraded through mitophagy to maintain local axon homeostasis. When the mitochondrial quality control mechanisms are broken down, SARM1 will cause irreversible damage for axon death.

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