Article
Biochemistry & Molecular Biology
Sierra R. Bruno, Amit Kumar, Zoe F. Mark, Ravishankar Chandrasekaran, Emily Nakada, Nicolas Chamberlain, Bethany Mihavics, Joseph Walzer, Jonathon Cahoon, Anne E. Dixon, Brian Cunniff, Vikas Anathy
Summary: Mitochondrial fission plays a significant role in the inflammatory response to allergens in asthma patients, leading to increased production of pro-inflammatory cytokines. The key gene responsible for regulating mitochondrial fission, DRP1, plays a crucial role in this process.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Medical Laboratory Technology
Yan Xia, Jiayu Jin, Ao Chen, Danbo Lu, Xinyu Che, Jiaqi Ma, Su Li, Ming Yin, Zheng Yang, Hao Lu, Chenguang Li, Jinxiang Chen, Muyin Liu, Yuan Wu, Hui Gong, Yunzeng Zou, Zhangwei Chen, Juying Qian, Junbo Ge
Summary: This study investigates the role of aspartate-glutamate carrier1 (AGC1) and dynamin-related protein 1 (Drp1) in mitochondrial fission and its contribution to doxorubicin (DOX)-induced cardiomyopathy. The results suggest that AGC1 regulates cardiac function through Drp1-mediated mitochondrial fission in dilated cardiomyopathy (DCM), and targeting the AGC1-Drp1 axis could be a potential therapeutic strategy for DOX-induced cardiomyopathy.
TRANSLATIONAL RESEARCH
(2023)
Article
Multidisciplinary Sciences
Lisa Tilokani, Fiona M. Russell, Stevie Hamilton, Daniel M. Virga, Mayuko Segawa, Vincent Paupe, Anja V. Gruszczyk, Margherita Protasoni, Luis -Carlos Tabara, Mark Johnson, Hanish Anand, Michael P. Murphy, D. Grahame Hardie, Franck Polleux, Julien Prudent
Summary: This study identifies MTFR1L as a critical mitochondrial protein that transduces AMPK-dependent metabolic changes through regulation of mitochondrial dynamics. The phosphorylation of MTFR1L by AMPK controls its function in regulating mitochondrial morphology and stress-induced AMPK-dependent mitochondrial fragmentation.
Article
Biochemistry & Molecular Biology
Fernanda Luisa Basei, Camila de Castro Ferezin, Ana Luisa Rodrigues de Oliveira, Juan Pablo Munoz, Antonio Zorzano, Jorg Kobarg
Summary: In this study, Nek4 is shown to regulate mitochondrial function, providing potential explanations for the co-occurrence of high mitochondrial respiration and mitochondrial fragmentation.
Article
Environmental Sciences
Nengzhou Chen, Zhenkun Guo, Zhousong Luo, Fuli Zheng, Wenya Shao, Guangxia Yu, Ping Cai, Siying Wu, Huangyuan Li
Summary: Long-term exposure to paraquat may increase the risk of Parkinson's disease, with ROS-mediated mitochondrial fission contributing to excessive mitophagy, which can be significantly ameliorated by mdivi-1.
ENVIRONMENTAL POLLUTION
(2021)
Article
Nanoscience & Nanotechnology
Boyue Huang, Liu Xie, Ming Ke, Yonghong Fan, Ju Tan, Jianhua Ran, Chuhong Zhu
Summary: Inhibition of METTL3-14 effectively reduces cardiomyocyte death and improves cardiac function and reduces fibrosis level. DPDMN delivers METTL3 inhibitor swiftly to rescue dying cardiomyocytes in the early phase and slowly suppresses fibroblast over proliferation and collagen synthesis in the late phase.
ACS APPLIED MATERIALS & INTERFACES
(2023)
Article
Biochemistry & Molecular Biology
Yu-Wang Chang, Zong-Han Song, Chien-Chang Chen
Summary: Loss of the mitochondrial fission enzyme Drp1 in cardiomyocytes can lead to energy shortage and heart failure. The study demonstrates that extracellular fibronectin and adrenergic agonists regulate mitochondrial morphology and function in cardiomyocytes through the FAK-ERK1/2-Drp1 pathway. Inhibition of this pathway can result in cellular energy shortage.
Article
Multidisciplinary Sciences
Shuaifeng Li, Shixun Han, Qi Zhang, Yibing Zhu, Haitao Zhang, Junli Wang, Yang Zhao, Jianhui Zhao, Lin Su, Li Li, Dawang Zhou, Cunqi Ye, Xin-Hua Feng, Tingbo Liang, Bin Zhao
Summary: The study reveals that elevated FUNDC2 causes mitochondrial fragmentation through inhibiting MFN1 in hepatocellular carcinoma. The findings suggest FUNDC2 as a potential therapeutic target for liver cancer.
NATURE COMMUNICATIONS
(2022)
Article
Pharmacology & Pharmacy
Yalin Zhang, Yilan Song, Chongyang Wang, Jingzhi Jiang, Siqi Liu, Qiaoyun Bai, Liangchang Li, Hainan Jin, Yongde Jin, Guanghai Yan
Summary: This study investigated the mechanism by which Panax notoginseng saponin (PNS-R1) attenuates allergic rhinitis (AR) through AMPK/Drp1-mediated mitochondrial fission. The results showed that PNS-R1 reduced allergic symptoms and inflammatory cytokine levels in AR mice, and improved immune imbalance. Additionally, PNS-R1 protected mitochondrial integrity by inhibiting mitochondrial fission and reducing apoptosis and ROS production.
BIOCHEMICAL PHARMACOLOGY
(2022)
Article
Cell Biology
Christina G. Towers, Darya K. Wodetzki, Jacqueline Thorburn, Katharine R. Smith, M. Cecilia Caino, Andrew Thorburn
Summary: This study investigated alternative forms of mitochondrial quality control beyond mitophagy to compensate for inactive autophagy. Rare surviving autophagy-deficient clones were found to adapt to maintain mitochondrial homeostasis through regulating mitochondrial dynamics and mitochondrial-derived vesicles. The research indicates unique dependencies of autophagy-dependent cells on these mechanisms to maintain mitochondrial health.
DEVELOPMENTAL CELL
(2021)
Article
Multidisciplinary Sciences
Maxime Boutry, Peter K. Kim
Summary: The study reveals that during mitochondrial division, the endoplasmic reticulum recruits lysosomes through the interaction of VAPs with ORP1L, creating a three-way contact between the ER, lysosomes, and mitochondria. Additionally, ORP1L may transport PI(4)P from lysosomes to mitochondria, demonstrating a direct role of PI(4)P in the fission process of mitochondria.
NATURE COMMUNICATIONS
(2021)
Article
Chemistry, Multidisciplinary
Chenyang Duan, Ruixue Liu, Lei Kuang, Zisen Zhang, Dongyao Hou, Danyang Zheng, Xinming Xiang, He Huang, Liangming Liu, Tao Li
Summary: This study reveals the mechanisms behind the formation of contacts between the endoplasmic reticulum and mitochondria following ischemia and hypoxia. It further demonstrates the crucial role of excessive mitochondrial fission and dysfunction in this process. Additionally, the study uncovers the involvement of cytoplasmic Drp1 in promoting ER-Mito contact initiation, as well as the interplay between related proteins and structures.
Article
Chemistry, Multidisciplinary
Xiao-long Li, Xue-wu Liu, Wei-ling Liu, Yu-quan Lin, Jing Liu, Yu-sheng Peng, Li-min Cheng, Yan-hua Du
Summary: TMEM16A expression is upregulated in acute kidney injury (AKI), and its inhibition can effectively prevent tubular cell apoptosis, inflammation, and kidney function loss induced by cisplatin. Additionally, TMEM16A inhibition can block mitochondrial fission through the ERK1/2/Drp1 pathway, thereby alleviating cisplatin-induced AKI.
ACTA PHARMACOLOGICA SINICA
(2023)
Article
Medicine, Research & Experimental
Keng-Mao Liao, Chih-Jung Chen, Wei-Jia Luo, Chen-Wei Hsu, Sung-Liang Yu, Pan-Chyr Yang, Kang-Yi Su
Summary: With an aging population and the numerous health impacts associated with old age, there is a growing need to find effective anti-aging drugs. In this study, diphenyleneiodonium (DPI) was identified as a potential anti-aging drug that promotes mitochondrial fission. DPI was found to reduce senescence-associated beta-galactosidase positive cells and increase proliferating cells. It also downregulated cell cycle arrest genes and SASP factors. DPI treatment in mice showed reduced senescence markers and improved physical impairments.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Multidisciplinary Sciences
Deepshikha Ghosh, Suman Pakhira, Damayanti Das Ghosh, Susanta Roychoudhury, Sib Sankar Roy
Summary: Ovarian cancer is a leading cause of cancer-related female mortality. Ets1, a transcription factor, promotes epithelial to mesenchymal transition (EMT) and serves as a potential malignancy marker in ovarian cancer. Our study reveals that Ets1 regulates mitochondrial fission-fusion dynamics by augmenting Drp1 through direct binding at the DNM1L (DRP1) promoter. Increased Drp1 levels due to Ets1 overexpression lead to reduced mitochondrial load and compromised ATP synthase expression, resulting in a shift towards glycolysis. Additionally, inhibiting mitochondrial fission through Drp1 inhibition mitigates Ets1-associated EMT in vitro and in vivo.