Emerging Role of Mitophagy in the Heart: Therapeutic Potentials to Modulate Mitophagy in Cardiac Diseases DOI Creative Commons
Yi Luan, Ying Luan, Feng Qi

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2021, Volume and Issue: 2021(1)

Published: Jan. 1, 2021

The normal function of the mitochondria is crucial for most tissues especially those that demand a high energy supply. Emerging evidence has pointed out healthy mitochondrial closely associated with heart function. When these processes fail to repair damaged mitochondria, cells initiate removal process referred as mitophagy clear away defective mitochondria. In cardiomyocytes, metabolic activity, cell differentiation, apoptosis, and other physiological involved in major phenotypic alterations. Mitophagy alterations may contribute detrimental or beneficial effects multitude cardiac diseases, indicating potential clinical insights after close understanding mechanisms. Here, we discuss current opinions progression such ischemic disease, diabetic cardiomyopathy, hypertrophy, failure, arrhythmia, focus on key molecules related pathways regulation mitophagy. We also recently reported approaches targeting therapy diseases.

Language: Английский

Regulated cell death in myocardial ischemia–reperfusion injury DOI
Q. Xiang, Xin Yi,

Xue‐Hai Zhu

et al.

Trends in Endocrinology and Metabolism, Journal Year: 2023, Volume and Issue: 35(3), P. 219 - 234

Published: Nov. 17, 2023

Language: Английский

Citations

128
Molecular Mechanisms of Mitochondrial Quality Control in Ischemic Cardiomyopathy DOI Creative Commons
Xing Chang, Ruxiu Liu, Ruibin Li

et al.

International Journal of Biological Sciences, Journal Year: 2022, Volume and Issue: 19(2), P. 426 - 448

Published: Dec. 19, 2022

Ischemic cardiomyopathy (ICM) is a special type of coronary heart disease or an advanced stage the disease, which related to pathological mechanism primary dilated cardiomyopathy. mainly occurs in long-term myocardial ischemia, resulting diffuse fibrosis. This turn affects cardiac ejection function, significant impact on systolic and diastolic decrease fraction. The pathogenesis ICM closely disease. Mainly due atherosclerosis caused by stenosis vascular occlusion, causing inflammatory lesions thrombosis. As progresses, it leads ischemia eventually ICM. mechanisms inflammation, hypertrophy, fibrosis remodeling. Mitochondria are organelles with double-membrane structure, so composition mitochondrial outer compartment basically similar that cytoplasm. When ischemia-reperfusion induces large influx calcium into cell, concentration ions also increases. subsequent opening membrane permeability transition pore inner overload homeostasis cardiomyocytes activates pathway apoptosis. Mitochondrial Quality Control (MQC), as important for regulating function cardiomyocytes, morphological structure/function lifespan mitochondria. In this review, we discuss role MQC (including mitophagy, dynamics, biosynthesis) provide evidence targeting

Language: Английский

Citations

81
Therapeutic strategies in ischemic cardiomyopathy: Focus on mitochondrial quality surveillance DOI
Xing Chang, Sam Toan, Ruibin Li

et al.

EBioMedicine, Journal Year: 2022, Volume and Issue: 84, P. 104260 - 104260

Published: Sept. 19, 2022

Language: Английский

Citations

77
TMBIM6 prevents VDAC1 multimerization and improves mitochondrial quality control to reduce sepsis-related myocardial injury DOI
Hao Zhou,

Zhe Dai,

Jialei Li

et al.

Metabolism, Journal Year: 2023, Volume and Issue: 140, P. 155383 - 155383

Published: Jan. 2, 2023

Language: Английский

Citations

55
Involvement of mitochondrial dynamics and mitophagy in diabetic endothelial dysfunction and cardiac microvascular injury DOI
Xiao Zhang, Hao Zhou,

Xing Chang

et al.

Archives of Toxicology, Journal Year: 2023, Volume and Issue: 97(12), P. 3023 - 3035

Published: Sept. 14, 2023

Language: Английский

Citations

42
Zishen Tongyang Huoxue decoction (TYHX) alleviates sinoatrial node cell ischemia/reperfusion injury by directing mitochondrial quality control via the VDAC1–β-tubulin signaling axis DOI
Xing Chang, Siyuan Zhou, Jinfeng Liu

et al.

Journal of Ethnopharmacology, Journal Year: 2023, Volume and Issue: 320, P. 117371 - 117371

Published: Nov. 18, 2023

Language: Английский

Citations

41
The E3 ubiquitin ligase MARCH2 protects against myocardial ischemia-reperfusion injury through inhibiting pyroptosis via negative regulation of PGAM5/MAVS/NLRP3 axis DOI Creative Commons

Shuolin Liu,

Yaguang Bi,

Tianting Han

et al.

Cell Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: Feb. 27, 2024

Inflammasome activation and pyroptotic cell death are known to contribute the pathogenesis of cardiovascular diseases, such as myocardial ischemia-reperfusion (I/R) injury, although underlying regulatory mechanisms remain poorly understood. Here we report that expression levels E3 ubiquitin ligase membrane-associated RING finger protein 2 (MARCH2) were elevated in ischemic human hearts or mouse upon I/R injury. Genetic ablation MARCH2 aggravated infarction cardiac dysfunction Single-cell RNA-seq analysis suggested loss prompted NLRP3 inflammasome cardiomyocytes. Mechanistically, phosphoglycerate mutase 5 (PGAM5) was found act a novel regulator MAVS-NLRP3 signaling by forming liquid-liquid phase separation condensates with MAVS fostering recruitment NLRP3. directly interacts PGAM5 promote its K48-linked polyubiquitination proteasomal degradation, resulting reduced PGAM5-MAVS co-condensation, consequently inhibition cardiomyocyte pyroptosis. AAV-based re-introduction significantly ameliorated I/R-induced heart dysfunction. Altogether, our findings reveal mechanism where MARCH2-mediated ubiquitination negatively regulates PGAM5/MAVS/NLRP3 axis protect against pyroptosis

Language: Английский

Citations

30
Mitochondrial quality control in human health and disease DOI Creative Commons
Bohao Liu,

Chen-Zhen Xu,

Yi Liu

et al.

Military Medical Research, Journal Year: 2024, Volume and Issue: 11(1)

Published: May 29, 2024

Abstract Mitochondria, the most crucial energy-generating organelles in eukaryotic cells, play a pivotal role regulating energy metabolism. However, their significance extends beyond this, as they are also indispensable vital life processes such cell proliferation, differentiation, immune responses, and redox balance. In response to various physiological signals or external stimuli, sophisticated mitochondrial quality control (MQC) mechanism has evolved, encompassing key like biogenesis, dynamics, mitophagy, which have garnered increasing attention from researchers unveil specific molecular mechanisms. this review, we present comprehensive summary of primary mechanisms functions regulators involved major components MQC. Furthermore, critical regulated by MQC its diverse roles progression systemic diseases been described detail. We discuss agonists antagonists targeting MQC, aiming explore potential therapeutic research prospects enhancing stabilize function.

Language: Английский

Citations

29
Mitochondrial Structure and Function in Human Heart Failure DOI
Antentor Hinton, Steven M. Claypool, Kit Neikirk

et al.

Circulation Research, Journal Year: 2024, Volume and Issue: 135(2), P. 372 - 396

Published: July 4, 2024

Despite clinical and scientific advancements, heart failure is the major cause of morbidity mortality worldwide. Both mitochondrial dysfunction inflammation contribute to development progression failure. Although crucial reparative healing following acute cardiomyocyte injury, chronic damages heart, impairs function, decreases cardiac output. Mitochondria, which comprise one third volume, may prove a potential therapeutic target for Known primarily energy production, mitochondria are also involved in other processes including calcium homeostasis regulation cellular apoptosis. Mitochondrial function closely related morphology, alters through dynamics, thus ensuring that needs cell met. However, failure, changes substrate use lead impaired myocyte function. This review discusses cristae role contact site organizing system complex ultrastructure changes. Additionally, this covers mitochondria-endoplasmic reticulum sites, communication via nanotunnels, altered metabolite production during We highlight these often-neglected factors promising targets

Language: Английский

Citations

27
Cardiovascular disease: Mitochondrial dynamics and mitophagy crosstalk mechanisms with novel programmed cell death and macrophage polarisation DOI Creative Commons
Dandan Liu,

Hewei Qin,

Yang Gao

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 206, P. 107258 - 107258

Published: June 21, 2024

Several cardiovascular illnesses are associated with aberrant activation of cellular pyroptosis, ferroptosis, necroptosis, cuproptosis, disulfidptosis and macrophage polarisation as hallmarks contributing to vascular damage abnormal cardiac function. Meanwhile, these three novel forms dysfunction closely related mitochondrial homeostasis. Mitochondria the main organelles that supply energy maintain Mitochondrial stability is maintained through a series regulatory pathways, such fission, fusion mitophagy. Studies have shown (e.g., impaired dynamics mitophagy) promotes ROS production, leading oxidative stress, which induces M1 phenotypic polarisation. Therefore, an in-depth knowledge dynamic regulation mitochondria during necessary understand disease development. This paper systematically summarises impact changes in mitophagy on regulating dysfunctions promote understanding pathogenesis diseases provide corresponding theoretical references for treating diseases.

Language: Английский

Citations

18