Jiabao Guo

North China University of Science and Technology

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Co-Authors

Jinkun Xi

North China University of Science and Technology

Yonggui He

North China University of Science and Technology

Tingting Ma

North China University of Science and Technology

Luyao Huang

Shandong University of Traditional Chinese Medicine

Ying Yang

Huazhong Agricultural University

Youcheng Hu

Wuhan University

Bohan Xing

North China University of Science and Technology

Pei Wang

Second Military Medical University

Pei Wang

Nanjing Agricultural University

Xiaoyi Li

North China University of Science and Technology

Cooperative Institutions

North China University of Science and Technology

Capital Medical University

First People's Hospital of Chongqing

North China University of Technology

In-Q-Tel

Tianjin Medical University

TED University

Yanbian University

Peking Union Medical College Hospital

Chinese Academy of Medical Sciences & Peking Union Medical College

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Resveratrol Inhibits Zinc Deficiency-Induced Mitophagy and Exerts Cardioprotective Effects

Research Square (Research Square) (2023)

Pei Wang Ying Yang Jiabao Guo Tingting Ma Youcheng Hu

Abstract Resveratrol (Res) has cardioprotective, anti-inflammatory, anti-aging and antioxidant effects; however, its mechanism remains unclear. Here we explored the protective effects of resveratrol on cardiomyocytes, focusing on the role of Zn 2+ and mitophagy. Using the MTT/LDH assay, we found that addition of a zinc chelator TPEN for 4h induced mitophagy and significantly reduced cell viability, increased cytotoxicity and apoptosis in H9c2, while Res significantly inhibited these effects of TPEN. Similarly, Res inhibited TPEN-induced expression of mitophagy-associated proteins P62, LC3, PINK1, Parkin and TOM20. The mitophagy inhibitor 3-MA blocked the function of Res. At the same time, we found that Mfn2 siRNA could reverse the inhibition of mitophagy by Res through AMPK (adenosine 5'-monophosphate (AMP)-activated protein kinase) and prevent the effect of the mitochondrial permeability transition pore (mPTP) opening. Thus, our data suggest that Res can exert mitochondrial protection by inhibiting mitophagy and preventing mPTP opening through AMPK-Mfn2 axis in myocardial cells.

PINK1

MPTP

MFN2

Viability assay

10.21203/rs.3.rs-2830934/v1

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Resveratrol Inhibits Zinc Deficiency-Induced Mitophagy and Exerts Cardiac Cytoprotective Effects

Biological Trace Element Research (2023)

Pei Wang Ying Yang Jiabao Guo Tingting Ma Youcheng Hu

MFN2

PINK1

MPTP

Viability assay

10.1007/s12011-023-03758-1

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Citations (9)

Zinc overload induces mitochondrial dysfunction and ROS-mediated mitophagy

Research Square (Research Square) (2023)

Ying Yang Pei Wang Jiabao Guo Tingting Ma Youcheng Hu

Abstract Zinc homeostasis is essential for maintaining redox balance, cell proliferation, and apoptosis. However, excessive zinc exposure is toxic and leads to mitochondrial dysfunction. In this study, we established a zinc overload model by treating rat cardiomyocyte H9c2 cells with ZnCl 2 at different concentrations. Our results showed that zinc overload increased LDH and reactive oxygen species (ROS) levels, leading to cell death, mitochondrial membrane potential decrease and impaired mitochondrial function and dynamics. Furthermore, zinc overload activated the PINK1/Parkin signaling pathway and induced mitochondrial autophagy via ROS, while NAC inhibited mitophagy and weakened the activation of PINK1/Parkin pathway, thereby preserving mitochondrial biogenesis. In addition, our data also showed that Mfn2 deletion increased ROS production and exacerbated cytotoxicity induced by zinc overload. Our results therefore suggest that ZnCl 2 -induced ROS generation causes mitochondrial autophagy and mitochondrial dysfunction, damaging H9c2 cardiomyocytes. Additionally, Mfn2 may play a key role in zinc ion-mediated endoplasmic reticulum and mitochondrial interactions.

MFN2

PINK1

Mitochondrial ROS

10.21203/rs.3.rs-3213158/v1

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Zn2+ protects H9C2 cardiomyocytes by alleviating MAMs-associated apoptosis and calcium signaling dysregulation

Cellular Signalling (2025)

Jiabao Guo Tingting Ma Bingyu Wang Bohan Xing Luyao Huang

Calcium Signaling

10.1016/j.cellsig.2025.111629

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