RETRACTED: Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

Zhang, Jing; Zhang, Feng; Wang, Yanou

doi:10.3389/fphys.2021.707634

Cited by 7 publications

(10 citation statements)

References 70 publications

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“…Similarly, hyperglycaemia increases mitochondria–ER contact and Ca 2+ levels in the ER and mitochondria of cardiomyocytes. However, Mfn2 silencing reduces mitochondria-ER cooperation, Ca 2+ concentrations in both ER and mitochondria, mitochondrial ROS production, ER stress and mitochondria-mediated apoptosis, preserving mitochondrial function and cardiomyocyte viability under hyperglycaemic conditions [ 45 ].…”

Section: Mitochondrial Dynamics In Dcmmentioning

confidence: 99%

The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy

Dabravolski

Sadykhov

Kartuesov

et al. 2022

IJMS

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Diabetic cardiomyopathy (DCM) is defined as the presence in diabetic patients of abnormal cardiac structure and performance (such as left ventricular hypertrophy, fibrosis, and arrhythmia) in the absence of other cardiac risk factors (such as hypertension or coronary artery disease). Although the pathogenesis of DCM remains unclear currently, mitochondrial structural and functional dysfunctions are recognised as a central player in the DCM development. In this review, we focus on the role of mitochondrial dynamics, biogenesis and mitophagy, Ca2+ metabolism and bioenergetics in the DCM development and progression. Based on the crucial role of mitochondria in DCM, application of mitochondria-targeting therapies could be effective strategies to slow down the progression of the disease.

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Section: Mitochondrial Dynamics In Dcmmentioning

confidence: 99%

The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy

Dabravolski

Sadykhov

Kartuesov

et al. 2022

IJMS

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“…DC is currently considered to be a cause of high mortality in patients with diabetes, and there is no effective treatment [65]. More and more studies indicate that ER stress is involved in DC [66][67][68]. Larry A. Barr and colleagues fed rats with a high-fat diet (HFD) to establish a diabetes rat model and then performed a series of experiments.…”

Section: Hydrogen Sulfide Improves Diabetic Cardiomyopathy By Regulat...mentioning

confidence: 99%

Hydrogen Sulfide Plays an Important Role by Regulating Endoplasmic Reticulum Stress in Diabetes-Related Diseases

Zhao

Liu

Yang

et al. 2022

IJMS

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Endoplasmic reticulum (ER) plays important roles in protein synthesis, protein folding and modification, lipid biosynthesis, calcium storage, and detoxification. ER homeostasis is destroyed by physiological and pharmacological stressors, resulting in the accumulation of misfolded proteins, which causes ER stress. More and more studies have shown that ER stress contributes to the pathogenesis of many diseases, such as diabetes, inflammation, neurodegenerative diseases, cancer, and autoimmune diseases. As a toxic gas, H2S has, in recent years, been considered the third most important gas signal molecule after NO and CO. H2S has been found to have many important physiological functions and to play an important role in many pathological and physiological processes. Recent evidence shows that H2S improves the body’s defenses to many diseases, including diabetes, by regulating ER stress, but its mechanism has not yet been fully understood. We therefore reviewed recent studies of the role of H2S in improving diabetes-related diseases by regulating ER stress and carefully analyzed its mechanism in order to provide a theoretical reference for future research.

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“…In recent years, studies have found that ER stress and mitochondrial apoptosis pathways may be involved in the progression of DCM, and myocardial cells in DCM patients are accompanied by glucose and lipid metabolism disorders, producing large amounts of reactive oxygen species (ROS). This leads to ER swelling and mitochondrial structure and function disorders, which in turn cause myocardial hypertrophy, interstitial fibrosis, myocardial necrosis, and apoptosis ( Zhou et al, 2018b ; Ljubkovic et al, 2019 ; Zhang J. et al, 2021 ).…”

Section: The Critical Role Of Endoplasmic Reticulum-mitochondria Contacts In Remodeling and Cardiovascular Remodeling-associated Diseasesmentioning

confidence: 99%

“…In addition, MAMs’ constitutive proteins may be involved in the pathogenesis of diabetic cardiomyopathy, for example, Mfn2 and FUNDC1. These protein bridges of MAMs could be potential therapeutic targets for DCM in the future ( Wu et al, 2019 ; Zhang J. et al, 2021 ). A recent work showed that Mfn2 promotes ERMCs in cardiomyocytes subjected to hyperglycemic conditions.…”

Section: The Critical Role Of Endoplasmic Reticulum-mitochondria Contacts In Remodeling and Cardiovascular Remodeling-associated Diseasesmentioning

confidence: 99%

“…Transmission electron microscopy micrographs suggested that Mfn2 silencing markedly increased the mean distance between the ER and the OMM ( Yuan M. et al, 2020 ). Additionally, Mfn2 deficiency decreased the production of mitochondrial ROS and the frequency of mitochondria-dependent apoptosis in cardiomyocytes ( Zhang J. et al, 2021 ). Therefore, the regulation of Mfn2-related MAMs may represent a potential therapeutic pathway for the treatment of DCM.…”

Section: The Critical Role Of Endoplasmic Reticulum-mitochondria Contacts In Remodeling and Cardiovascular Remodeling-associated Diseasesmentioning

confidence: 99%

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Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases

Wang

Zhang

Wen

et al. 2021

Front. Cell Dev. Biol.

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Cardiovascular remodeling occurs in cardiomyocytes, collagen meshes, and vascular beds in the progress of cardiac insufficiency caused by a variety of cardiac diseases such as chronic ischemic heart disease, chronic overload heart disease, myocarditis, and myocardial infarction. The morphological changes that occur as a result of remodeling are the critical pathological basis for the occurrence and development of serious diseases and also determine morbidity and mortality. Therefore, the inhibition of remodeling is an important approach to prevent and treat heart failure and other related diseases. The endoplasmic reticulum (ER) and mitochondria are tightly linked by ER-mitochondria contacts (ERMCs). ERMCs play a vital role in different signaling pathways and provide a satisfactory structural platform for the ER and mitochondria to interact and maintain the normal function of cells, mainly by involving various cellular life processes such as lipid metabolism, calcium homeostasis, mitochondrial function, ER stress, and autophagy. Studies have shown that abnormal ERMCs may promote the occurrence and development of remodeling and participate in the formation of a variety of cardiovascular remodeling-associated diseases. This review focuses on the structure and function of the ERMCs, and the potential mechanism of ERMCs involved in cardiovascular remodeling, indicating that ERMCs may be a potential target for new therapeutic strategies against cardiovascular remodeling-induced diseases.

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RETRACTED: Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

Cited by 7 publications

References 70 publications

The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy

The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy

Hydrogen Sulfide Plays an Important Role by Regulating Endoplasmic Reticulum Stress in Diabetes-Related Diseases

Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases

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