Article
Cell Biology
James L. Shen, Tina M. Fortier, Ruoxi Wang, Eric H. Baehrecke
Summary: Defects in autophagy can lead to issues in metabolism, development, and disease. The loss of Vps13D affects mitophagy, regulated by the core autophagy machinery. Pink1 and Vps13D play roles in Pink1-dependent mitophagy, with Park contributing to mitochondrial clearance through a pathway parallel to Vps13D.
JOURNAL OF CELL BIOLOGY
(2021)
Review
Neurosciences
Hezhou Han, Sainan Hu, Yue Hu, Dongliang Liu, Junbo Zhou, Xiaofang Liu, Xiulan Ma, Yaodong Dong
Summary: Mitochondrial dysfunction is associated with ototoxicity caused by external factors. The regulation of mitophagy, through key mitophagy regulatory proteins and signaling pathways, plays a crucial role in maintaining mitochondrial homeostasis and function. Recent investigations on the control of cell fate by mitophagy have improved our understanding of the mechanisms underlying ototoxicity and other hearing-related diseases, offering potential opportunities for targeted mitochondrial therapies in the treatment of ototoxicity.
FRONTIERS IN CELLULAR NEUROSCIENCE
(2023)
Article
Biochemistry & Molecular Biology
Paola Lenzi, Rosangela Ferese, Francesca Biagioni, Federica Fulceri, Carla L. Busceti, Alessandra Falleni, Stefano Gambardella, Alessandro Frati, Francesco Fornai
Summary: The study reveals that GBM cells exhibit mitochondrial alterations associated with mTOR overexpression and autophagy suppression, and the administration of mTOR inhibitor rapamycin can rescue these mitochondrial alterations. Rapamycin induces the expression of genes promoting mitophagy and mitochondrial fission, along with increased expression of VPS34, restoring healthy mitochondria in GBM cells. The findings provide novel evidence about mitochondria in GBM and suggest a potential therapeutic approach through mTOR inhibition to restore healthy mitochondria.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Chemistry, Multidisciplinary
Guy Mann, Gandhesiri Satish, Prasad Sulkshane, Shaswati Mandal, Michael H. Glickman, Ashraf Brik
Summary: Protein post-translational modifications play a crucial role in cellular signaling, but their study in human cells is limited. This study presents the first synthesis, delivery, and cellular study of a stable phosphoubiquitin probe, allowing for direct visualization of Parkin's substrate preference during mitophagy.
CHEMICAL COMMUNICATIONS
(2021)
Article
Plant Sciences
De Zhao Kong, Peng Sun, Yi Lu, Ye Yang, Dong Yu Min, Si Cheng Zheng, Yi Yang, Zhe Zhang, Guan Lin Yang, Jun Wen Jiang
Summary: Yi Mai granule (YMG) has therapeutic effects in improving mitochondrial autophagy and alleviating cardiovascular disease possibly by regulating the Pink1-Mfn2-Parkin pathway via miRNA-125a-5p and regulating proinflammatory factors, vasoconstriction cytokines, and blood lipids to alleviate atherosclerosis.
JOURNAL OF ETHNOPHARMACOLOGY
(2024)
Article
Biochemistry & Molecular Biology
Marta Vranas, Yang Lu, Shafqat Rasool, Nathalie Croteau, Jonathan D. Krett, Veronique Sauve, Kalle Gehring, Edward A. Fon, Thomas M. Durcan, Jean-Francois Trempe
Summary: Mutations in Parkin and PINK1 cause early-onset familial Parkinson's disease. The study found that His433 contributes to the catalysis of Parkin and its mutation impairs mitophagy. Mfn2 is a kinetically preferred substrate for Parkin, co-localizing with PINK1 and phospho-ubiquitin upon mitochondrial depolarization.
Review
Biochemistry & Molecular Biology
Chi-Jing Choong, Hideki Mochizuki, Cesar Borlongan
Summary: Mitochondrial dysregulation is strongly associated with the pathogenesis of Parkinson's disease (PD), with mutated genes affecting mitochondrial features. Disruption of mitochondrial quality control and abnormal secretion of mitochondrial contents play a role in PD, and circulating mitochondrial DNAs can elicit inflammatory response.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Neurosciences
Iryna Kamienieva, Jerzy Duszynski, Joanna Szczepanowska
Summary: The familial form of Parkinson's disease is linked to mutations in specific genes, with mutations in the parkin gene being one of the most common causes of early-onset PD. Mitochondrial dysfunction is an emerging active player in the pathology of neurodegenerative diseases, as mitochondria are highly dynamic structures integrated with many cellular functions.
TRANSLATIONAL NEURODEGENERATION
(2021)
Article
Medicine, Research & Experimental
Zhuangzhuang Jin, Bohan Chang, Yingliang Wei, Yue Yang, He Zhang, Jiabao Liu, Longhuan Piao, Lunhao Bai
Summary: Curcumin, with its anti-inflammatory and antioxidant properties, shows potential therapeutic value in the treatment of osteoarthritis. Through analyzing the action targets of curcumin, the study found that curcumin attenuates osteoarthritis characteristics by activating mitophagy. These findings highlight the importance of mitophagy in the treatment of osteoarthritis with curcumin.
BIOMEDICINE & PHARMACOTHERAPY
(2022)
Article
Pharmacology & Pharmacy
Jian Sun, Fan Yu, Tao Wang, Jianchun Bian, Zongping Liu, Hui Zou
Summary: Cadmium is an important environmental pollutant that causes damage to multiple systems of the body. This study found that cadmium damages liver cells, disrupts the structure and function of mitochondria, and increases the production of superoxide anions. It was also discovered that cadmium increases mitochondrial division and induces mitophagy through the PINK1-Parkin pathway. Mitophagy plays a protective role in early cadmium-induced liver damage.
Article
Cell Biology
Haixia Wen, Luxi Li, Lixuan Zhan, Yunyan Zuo, Kongping Li, Meiqian Qiu, Heying Li, Weiwen Sun, En Xu
Summary: The study showed that hypoxic postconditioning (HPC) exerts neuroprotection against transient global cerebral ischemia (tGCI) by promoting mitophagy mediated by the PINK1/Parkin-dependent pathway in the hippocampal CA1 subregion. This novel finding provides a new perspective on neuroprotection mechanisms against cerebral ischemia.
CELL DEATH & DISEASE
(2021)
Article
Clinical Neurology
Xu Hou, Jens O. Watzlawik, Casey Cook, Chia-Chen Liu, Silvia S. Kang, Wen-Lang Lin, Michael DeTure, Michael G. Heckman, Nancy N. Diehl, Fadi S. Hanna Al-Shaikh, Ronald L. Walton, Owen A. Ross, Heather L. Melrose, Nilufer Ertekin-Taner, Guojun Bu, Leonard Petrucelli, John D. Fryer, Melissa E. Murray, Dennis W. Dickson, Fabienne C. Fiesel, Wolfdieter Springer
Summary: The study reveals alterations in mitophagy in AD that are associated with early tau pathology, suggesting that distinct mitochondrial, autophagic, and/or lysosomal failures may contribute to the selective vulnerability in the disease.
ALZHEIMERS & DEMENTIA
(2021)
Review
Cell Biology
Xiusheng Chen, Qi Wang, Shihua Li, Xiao-Jiang Li, Weili Yang
Summary: PINK1 is a mitochondrial kinase involved in mitophagy and neuronal protection. Mutations in PINK1 gene can cause early onset Parkinson's disease with mitochondrial dysfunction. Although there is evidence from in vitro studies supporting the role of PINK1 in regulating mitochondrial function, strong in vivo evidence is still lacking. Additionally, PINK1 has functions independent of mitochondria.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Cell Biology
Ian G. Ganley, Anne Simonsen
Summary: Mitochondria are crucial for cellular processes and are targeted for degradation through autophagy, but the mechanisms and importance of this process are not well understood.
JOURNAL OF CELL SCIENCE
(2022)
Review
Biochemistry & Molecular Biology
Rajesh Kumar, Andreas S. Reichert
Summary: Mitochondria are essential organelles in eukaryotic cells involved in various cellular functions, and dysfunction is linked to several diseases. Both yeast and mammals utilize similar mechanisms to regulate mitophagy, a process of degrading damaged mitochondria.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)