Article
Cell Biology
Biting Zhou, Lijun Fang, Yanli Dong, Juhua Yang, Xiaole Chen, Nanwen Zhang, Yihua Zhu, Tianwen Huang
Summary: Activation of both mitophagy and mtUPR pathways can protect against oxidative injury in RDDs by increasing cell viability, reducing apoptosis and oxidative damage levels, as well as maintaining mitochondrial function. These pathways serve as potential therapeutic targets to delay the progression of RDDs by enhancing mitochondrial proteostasis.
CELL DEATH & DISEASE
(2021)
Review
Cell Biology
Varun Kumar, Ula V. Jurkunas
Summary: Fuchs Endothelial Corneal Dystrophy (FECD) is a genetically complex, age-related degenerative disease characterized by protein deposition in the cornea that leads to glare and visual complaints. Mitochondrial dysfunction and mitophagy play critical roles in the pathogenesis of FECD.
Article
Multidisciplinary Sciences
Philippe Vangrieken, Salwan Al-Nasiry, Aalt Bast, Pieter A. Leermakers, Christy B. M. Tulen, Ger. M. J. Janssen, Iris Kaminski, Iris Geomini, Titus Lemmens, Paul M. H. Schiffers, Frederik J. van Schooten, Alex H. V. Remels
Summary: The study found that placental hypoxia resulted in mitochondrial-generated reactive oxygen species and significant alterations in the molecular pathways controlling mitochondrial content and function. Targeting mitochondrial oxidative stress may have therapeutic benefit in managing pathologies related to placental hypoxia.
Article
Medicine, Research & Experimental
Chayodom Maneechote, Thawatchai Khuanjing, Benjamin Ongnok, Apiwan Arinno, Nanthip Prathumsap, Titikorn Chunchai, Busarin Arunsak, Wichwara Nawara, Siriporn C. Chattipakorn, Nipon Chattipakorn
Summary: The study reveals that modulating mitochondrial dynamics can protect the heart from doxorubicin-induced cardiotoxicity. Inhibiting mitochondrial fission or promoting fusion can alleviate the deterioration of mitochondrial function and dynamic regulation caused by doxorubicin, and mitigate oxidative stress, inflammation, myocardial injury, apoptosis, autophagy, and mitochondrial respiration.
Article
Cell Biology
Jinfa Ma, Lei Liu, Lu Song, Jianghong Liu, Lingyao Yang, Quan Chen, Jane Y. Wu, Li Zhu
Summary: This study reveals the mechanism of mitochondrial import of TDP-43 and the active role played by mitochondria in regulating TDP-43 homeostasis. FUNDC1 gene, a mitophagy receptor, is found to be co-expressed with TDP-43 and promotes mitochondrial translocation of TDP-43. Overexpressing FUNDC1 enhances TDP-43 induced mitochondrial damage, while down-regulating FUNDC1 reverses it, suggesting FUNDC1's involvement in regulating mitochondrial TDP-43 import and degradation.
CELL DEATH & DISEASE
(2023)
Article
Biochemistry & Molecular Biology
Maria Jose Perez, Dina Ivanyuk, Vasiliki Panagiotakopoulou, Gabriele Di Napoli, Stefanie Kalb, Dario Brunetti, Rawaa Al-Shaana, Stephan A. Kaeser, Sabine Anne-Kristin Fraschka, Mathias Jucker, Massimo Zeviani, Carlo Viscomi, Michela Deleidi
Summary: Mutations in the PITRM1 gene lead to a slow-progressing syndrome characterized by cerebellar ataxia and cognitive decline. Studies using PITRM1-knockout iPSCs show induction of mitochondrial unfolded protein response and increased mitochondrial clearance in neurons, as well as elevated levels of amyloid precursor protein and amyloid beta. Astrocytes also show dysregulated immune transcriptional signatures in PITRM1-knockout cerebral organoids.
MOLECULAR PSYCHIATRY
(2021)
Article
Endocrinology & Metabolism
Jay Kumar, Ghulam Mohammad, Kumari Alka, Renu A. Kowluru
Summary: Mitochondrial dysfunction plays a critical role in the development of diabetic retinopathy. Hyperglycemia downregulates the mtDNA-encoded LncRNA cytochrome B (LncCytB) in retinal endothelial cells, leading to impaired mtDNA packaging and increased vulnerability to damage.
Article
Obstetrics & Gynecology
Philippe Vangrieken, Salwan Al-Nasiry, Aalt Bast, Pieter A. Leermakers, Christy B. M. Tulen, Paul M. H. Schiffers, Frederik J. van Schooten, Alex H. V. Remels
Summary: Preeclamptic placentae exhibit oxidative stress, mitochondrial abnormalities, and inflammation, leading to decreased mitochondrial content and dysregulation of molecular pathways, which may contribute to the pathophysiology of preeclampsia.
REPRODUCTIVE SCIENCES
(2021)
Article
Cell Biology
Lorenzo Franci, Alessandro Tubita, Franca Maria Bertolino, Alessandro Palma, Giuseppe Cannino, Carmine Settembre, Andrea Rasola, Elisabetta Rovida, Mario Chiariello
Summary: This study demonstrates the important role of MAPK15 in cellular senescence by controlling mitophagy and preventing oxidative stress and nuclear DNA damage. MAPK15 protects cells from age-related diseases by maintaining mitochondrial quality through efficient disposal of old and damaged organelles.
Article
Biochemistry & Molecular Biology
Li Shu, Chao Hu, Meng Xu, Jianglong Yu, He He, Jie Lin, Hongying Sha, Bin Lu, Simone Engelender, Minxin Guan, Zhiyin Song
Summary: Mitochondrial DNA is susceptible to damage, especially under oxidative stress. A newly identified mitophagy receptor, ATAD3B, promotes the clearance of damaged mtDNA induced by oxidative stress. ATAD3B hetero-oligomerizes with ATAD3A under normal conditions, but oxidative stress-induced mtDNA damage disrupts this interaction and triggers mitophagy.
Article
Biochemistry & Molecular Biology
Craig K. Docherty, Jordan Bresciani, Andy Carswell, Amrita Chanderseka, Elaine Friel, Marianna Stasi, John R. Mercer
Summary: The study found that Pink1 plays a crucial role in the energetic metabolism of vascular smooth muscle cells, and knockout of Pink1 affects the development of plaque quality in atherosclerosis by reducing VSMC and extracellular matrix components.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Environmental Sciences
He Bai, Fan Yang, Wenjuan Jiang, Aiming Hu, Huifeng Chang, Yiling Zhang, Lu Jiang, Shixuan Lin, Zengting Lu, Caiying Zhang, Huabin Cao
Summary: This study elucidates that co-exposure to Mo and Cd can induce oxidative stress and mitophagy in Hepa1-6 cells through the ROS-mediated PINK1/Parkin pathway, with inhibition of mitophagy exacerbating the mitochondrial dysfunction induced by Mo and Cd.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2021)
Review
Biochemistry & Molecular Biology
Yu Liu, Yuejia Huang, Chong Xu, Peng An, Yongting Luo, Lei Jiao, Junjie Luo, Yongzhi Li
Summary: Mitochondrial dysfunction plays a significant role in the pathogenesis of CVDs, with mtDNA mutations being a key factor. Strategies such as eliminating mtDNA mutations, enhancing mitophagy, improving OXPHOS capacity, and reducing ROS offer potential therapeutic approaches for CVDs. However, there are limitations to current treatment strategies.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Environmental Sciences
Yu Shang, Wanlei Xue, Jiexing Kong, Yingjun Chen, Xinghua Qiu, Xingqin An, Yi Li, Hongli Wang, Jing An
Summary: This study found that exposure to ambient ultrafine black carbon causes mitochondrial oxidative stress, leading to mitochondrial dysfunction and neurotoxicity. Regulation of mitophagy process can mitigate mitochondrial damage.
SCIENCE OF THE TOTAL ENVIRONMENT
(2022)
Editorial Material
Cell Biology
Jonathan M. Palozzi, Thomas R. Hurd
Summary: Female germline has evolved a programmed germline mitophagy (PGM) to control the quality of mitochondrial DNA (mtDNA). PGM is induced by the inhibition of mTorC1 and requires the autophagy machinery and the mitophagy adaptor BNIP3, but not Pink1 and park, for germline mtDNA quality control. The study also identified Atx2 as a major regulator of PGM.
Article
Cell & Tissue Engineering
Guo-Qing Chen, Ping Ye, Rong-Song Ling, Fa Zeng, Xiong-Shan Zhu, Lu Chen, Yan Huang, Ling Xu, Xiao-Ying Xie
STEM CELLS INTERNATIONAL
(2020)
Article
Biotechnology & Applied Microbiology
GuoQing Chen, Lu Chen, Yan Huang, XiongShan Zhu, YuanLan Yu
Summary: This study investigates the role of FUNDC1 ubiquitination level in mitophagy and injury in hypoxic trophoblast cells. The low ubiquitination level of FUNDC1 in hypoxic trophoblast cells and placenta of pregnant women with PE was observed. Inhibition of FUNDC1 ubiquitination promoted mitophagy and mitochondrial membrane potential in normoxic trophoblast cells, and alleviated oxidative injury in PE mice.