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

The role of glycolytic metabolic pathways in cardiovascular disease and potential therapeutic approaches DOI Creative Commons
Shuxian Chen, Yuanming Zou, Chunyu Song

et al.

Basic Research in Cardiology, Journal Year: 2023, Volume and Issue: 118(1)

Published: Nov. 8, 2023

Abstract Cardiovascular disease (CVD) is a major threat to human health, accounting for 46% of non-communicable deaths. Glycolysis conserved and rigorous biological process that breaks down glucose into pyruvate, its primary function provide the body with energy intermediate products needed life activities. The non-glycolytic actions enzymes associated glycolytic pathway have long been found be development CVD, typically exemplified by metabolic remodeling in heart failure, which condition exhibits rapid adaptive response hypoxic conditions, occurring early course failure. It mainly characterized decrease oxidative phosphorylation rise pathway, glycolysis considered hallmark remodeling. In addition this, main source cardiomyocytes during ischemia–reperfusion. Not only that, auxiliary pathways glycolysis, such as polyol hexosamine pentose phosphate are also closely related CVD. Therefore, targeting very attractive therapeutic intervention However, relationship between CVD complex, some preclinical studies confirmed does certain degree efficacy, but specific role has yet explored. This article aims summarize current knowledge regarding key (including hexokinase (HK), phosphoglucose isomerase (PGI), phosphofructokinase-1 (PFK1), aldolase (Aldolase), phosphoglycerate metatase (PGAM), enolase (ENO) pyruvate kinase (PKM) lactate dehydrogenase (LDH)) their cardiovascular diseases (e.g., myocardial infarction, atherosclerosis) possible emerging targets.

Language: Английский

Citations

23

The crosstalk between mitochondrial quality control and metal-dependent cell death DOI Creative Commons

Qi-yuan Zhou,

Chao Ren,

Jing‐Yan Li

et al.

Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(4)

Published: April 27, 2024

Abstract Mitochondria are the centers of energy and material metabolism, they also serve as storage dispatch hubs metal ions. Damage to mitochondrial structure function can cause abnormal levels distribution ions, leading cell dysfunction even death. For a long time, quality control pathways such dynamics mitophagy have been considered inhibit metal-induced However, with discovery new metal-dependent death including ferroptosis cuproptosis, increasing evidence shows that there is complex relationship between This article reviews latest research results mechanisms crosstalk in recent years, well their involvement neurodegenerative diseases, tumors other order provide ideas for treatment related diseases.

Language: Английский

Citations

11

The dual role of PGAM5 in inflammation DOI Creative Commons

Yuxin Qi,

Bhavana Rajbanshi,

Ruihan Hao

et al.

Experimental & Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 10, 2025

Abstract In recent years, the focus on human inflammation in research has increased, with aging-related widely recognized as a defining characteristic of aging. Inflammation is strongly correlated mitochondrial dysfunction. Phosphoglycerate mutase family member 5 (PGAM5) novel modulator homeostasis response to mechanical stimulation. Here we review structure and sublocalization PGAM5, introduce its importance programmed cell death summarize crucial roles development progression inflammatory diseases such pneumonia, hepatitis, neuroinflammation Notably, PGAM5 dual effects controlling inflammation: distinct PGAM5-mediated functions exhibit cellular heterogeneity, leading control. We therefore highlight double-edged sword nature potential critical regulator innovative therapeutic target inflammation. Finally, challenges future directions use which properties, molecule clinic are discussed. This provides insights guide intelligent strategies targeting PGAM5-specific regulation treat intractable conditions, well extension broader application other achieve more precise effective treatment outcomes.

Language: Английский

Citations

1

SIRT1 Alleviates Mitochondrial Fission and Necroptosis in Cerebral Ischemia/Reperfusion Injury via SIRT1–RIP1 Signaling Pathway DOI Creative Commons
Xuan Wei,

Hanjing Guo,

Guangshan Huang

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: Feb. 24, 2025

ABSTRACT Programmed cell death, including necroptosis, plays a critical role in the pathogenesis of cerebral ischemia/reperfusion injury (CIRI). Silent information regulator 1 (SIRT1) has been identified as potential therapeutic target for CIRI, yet its precise regulating necroptosis remains controversial. Furthermore, interaction between SIRT1 and receptor‐interacting protein kinase (RIP1) this context is not fully understood. Sanpian Decoction (SPD), classical traditional herbal formula, was previously shown to enhance expression our studies. Our findings demonstrated that, both vivo vitro, CIRI associated with decrease levels phosphorylated dynamin‐related (p‐DRP1) at Ser637, alongside an increase RIP1 other necroptosis‐related proteins. Co‐immunoprecipitation immunofluorescence analyses revealed weakened RIP1. abnormal mitochondrial fission dysfunction were mediated through phosphoglycerate mutase 5–DRP1 pathway. Notably, SPD treatment improved neurological outcomes reversed these pathological changes by enhancing SIRT1–RIP1 interaction. In conclusion, study suggests that promising capable inhibiting mitigating via exhibits activating SIRT1, thereby attenuating during CIRI.

Language: Английский

Citations

1

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

Citations

53