Mitophagy in atherosclerosis: from mechanism to therapy

Zhang, Yanhong; Weng, Jiajun; Huan, Luyao; Sheng, Song; Xu, Fei

doi:10.3389/fimmu.2023.1165507

Cited by 15 publications

(8 citation statements)

References 376 publications

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“…One origin of excess mtROS is damaged mitochondria, which are prone to shifting mitochondrial dynamics to fission, resulting in an overload of mitochondrial fragments. Therefore, a highly efficient mechanism of removing damaged mitochondria exists, i.e., mitophagy, to maintain mitochondrial health, which is of particular value for the cardiovascular system [143,144].…”

Section: Mitochondrial Dysfunction In Endothelial Cellsmentioning

confidence: 99%

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Kulovic-Sissawo,

Tocantins,

Diniz

et al. 2024

Biology

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Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative diseases, and it contributes significantly to the global health burden. Recent research indicates a link between cardiovascular risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, and endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are recruited into the vessel wall to maintain appropriate endothelial function, repair, and angiogenesis. After attachment, EPCs differentiate into mature endothelial cells (ECs). Like ECs, EPCs are also susceptible to CVRFs, including metabolic dysfunction and chronic inflammation. Therefore, mitochondrial dysfunction of EPCs may have long-term effects on the function of the mature ECs into which EPCs differentiate, particularly in the presence of endothelial damage. However, a link between CVRFs and impaired mitochondrial function in EPCs has hardly been investigated. In this review, we aim to consolidate existing knowledge on the development of mitochondrial and endothelial dysfunction in the vascular endothelium, place it in the context of recent studies investigating the consequences of CVRFs on EPCs, and discuss the role of mitochondrial dysfunction. Thus, we aim to gain a comprehensive understanding of mechanisms involved in EPC deterioration in relation to CVRFs and address potential therapeutic interventions targeting mitochondrial health to promote endothelial function.

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Section: Mitochondrial Dysfunction In Endothelial Cellsmentioning

confidence: 99%

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Kulovic-Sissawo,

Tocantins,

Diniz

et al. 2024

Biology

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“…Recent studies have focused on targeting mitophagy to treat VC, a representative lesion in atherosclerosis. Mitophagy, a form of autophagy, selectively removes dysfunctional and depolarized mitochondria to maintain mitochondrial function and cellular homeostasis [51].…”

Section: Mitophagy As a Potential Therapeutic Target For Vascular Cal...mentioning

confidence: 99%

Role of PTEN-Induced Protein Kinase 1 as a Mitochondrial Dysfunction Regulator in Cardiovascular Disease Pathogenesis

Gwon,

Lee

2024

Vasc Specialist Int

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Cardiovascular disease (CVD) remains a global health challenge, primarily due to atherosclerosis, which leads to conditions such as coronary artery disease, cerebrovascular disease, and peripheral arterial disease. Mitochondrial dysfunction initiates endothelial dysfunction, a key contributor to CVD pathogenesis, as well as triggers the accumulation of reactive oxygen species (ROS), energy stress, and cell death in endothelial cells, which are crucial for atherosclerosis development. This review explores the role of PTEN-induced protein kinase 1 (PINK1) in mitochondrial quality control, focusing on its significance in cardiovascular health. PINK1 plays a pivotal role in mitophagy (selective removal of damaged mitochondria), contributing to the prevention of CVD progression. PINK1-mediated mitophagy also affects the maintenance of cardiomyocyte homeostasis in ischemic heart disease, thus mitigating mitochondrial dysfunction and oxidative stress, as well as regulates endothelial health in atherosclerosis through influencing ROS levels and inflammatory response. We also investigated the role of PINK1 in vascular smooth muscle cells, emphasizing on its role in apoptosis and atherosclerosis. Dysfunctional mitophagy in these cells accelerates cellular senescence and contributes to adverse effects including plaque rupture and inflammation. Mitophagy has also been explored as a potential therapeutic target for vascular calcification, a representative lesion in atherosclerosis, with a focus on lactate-induced mechanisms. Finally, we highlight the current research and clinical trials targeting mitophagy as a therapeutic avenue for CVD.

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“…Autophagy plays a crucial role in regulating ROS and NO productions in ECs. In general, autophagy acts as an antioxidative mechanism by removing damaged mitochondria in a process of mitophagy and other cellular components that generate excessive ROS [ 169 ]. The inhibition of autophagy disrupts the delicate balance between ROS production and clearance, leading to exacerbated oxidative stress and endothelial dysfunction [ 170 ].…”

Section: Autophagy In Cardiac Muscle Cellsmentioning

confidence: 99%

Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications

Bielawska,

Warszyńska,

Stefańska

et al. 2023

JCDD

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Autophagy, a dynamic and complex process responsible for the clearance of damaged cellular components, plays a crucial role in maintaining myocardial homeostasis. In the context of heart failure, autophagy has been recognized as a response mechanism aimed at counteracting pathogenic processes and promoting cellular health. Its relevance has been underscored not only in various animal models, but also in the human heart. Extensive research efforts have been dedicated to understanding the significance of autophagy and unravelling its complex molecular mechanisms. This review aims to consolidate the current knowledge of the involvement of autophagy during the progression of heart failure. Specifically, we provide a comprehensive overview of published data on the impact of autophagy deregulation achieved by genetic modifications or by pharmacological interventions in ischemic and non-ischemic models of heart failure. Furthermore, we delve into the intricate molecular mechanisms through which autophagy regulates crucial cellular processes within the three predominant cell populations of the heart: cardiomyocytes, cardiac fibroblasts, and endothelial cells. Finally, we emphasize the need for future research to unravel the therapeutic potential associated with targeting autophagy in the management of heart failure.

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Mitophagy in atherosclerosis: from mechanism to therapy

Cited by 15 publications

References 376 publications

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Role of PTEN-Induced Protein Kinase 1 as a Mitochondrial Dysfunction Regulator in Cardiovascular Disease Pathogenesis

Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications

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