Article
Cell Biology
Guang Lu, Hayden Weng Siong Tan, Tomas Schmauck-Medina, Liming Wang, Jiaqing Chen, Yik-Lam Cho, Kelie Chen, Jing-Zi Zhang, Weifeng He, Yihua Wu, Dajing Xia, Jing Zhou, Evandro F. Fang, Lei Fang, Wei Liu, Han-Ming Shen
Summary: This study reveals the crucial role of WIPI2 in mitochondrial recruitment of VCP to promote outer mitochondrial membrane protein degradation and eventual mitophagy. WIPI2 is recruited to damaged mitochondria upon mitophagy induction and its loss impairs mitophagy induced by mitochondrial damaging agents. WIPI2 binds to and promotes the transportation of AAA-ATPase VCP/p97 to damaged mitochondria, and its depletion blunts the recruitment of VCP to damaged mitochondria, leading to reduction in degradation of outer mitochondrial membrane proteins and mitophagy. Furthermore, WIPI2 is implicated in cell fate decision as cells deficient in WIPI2 are largely resistant to cell death induced by mitochondrial damage.
Article
Biochemistry & Molecular Biology
Shuang Li, Qian Xin, Guangyao Fang, Yi Deng, Fengyuan Yang, Chenming Qiu, Yongjian Yang, Cong Lan
Summary: Physical exercise can prevent cardiac hypertrophy by upregulating mitochondrial TERT expression. Overexpression of mitochondrial-targeted TERT improves mitochondrial dysfunction and reduces oxidative stress, leading to the attenuation of cardiac hypertrophy.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2024)
Article
Cell Biology
Zhengying Yu, Haipeng Wang, Wanyi Tang, Shaoyang Wang, Xiaoying Tian, Yujie Zhu, Hao He
Summary: A new optical method, UPLaS, has been developed to precisely and noninvasively induce localized mitochondrial Ca2+ oscillations, which directly initiates the PINK1-Parkin pathway for mitophagy.
CELL DEATH & DISEASE
(2021)
Article
Multidisciplinary Sciences
Huan Yang, Caroline Sibilla, Raymond Liu, Jina Yun, Bruce A. Hay, Craig Blackstone, David C. Chan, Robert J. Harvey, Ming Guo
Summary: This study identifies Clueless and CLUH as key regulators of Drp1, which control mitochondrial fission and have important impacts on cellular functions.
NATURE COMMUNICATIONS
(2022)
Article
Biochemistry & Molecular Biology
Chang-Yong Choi, Mai Tram Vo, John Nicholas, Young Bong Choi
Summary: Our study reveals that the mitochondrial translation elongation factor Tu located on the outer membrane of mitochondria can inhibit altered mitochondria-induced apoptosis through its autophagic function. The autophagy-competent TUFM is required for self-dimerization and mitophagy, and its stabilization upon autophagy activation could inhibit caspase-8 activation, providing insights into the regulation of apoptosis by mitophagy.
CELL DEATH AND DIFFERENTIATION
(2022)
Article
Cell Biology
Elizabeth M. Connelly, Karling S. Frankel, Gary S. Shaw
Summary: Aging, toxic chemicals, and changes to cellular environment cause oxidative damage to mitochondria, contributing to neurodegenerative diseases like Parkinson's. To maintain homeostasis, cells use signaling mechanisms involving PINK1 and parkin to identify and remove damaged proteins and mitochondria. PINK1 phosphorylates ubiquitin on mitochondrial proteins in response to oxidative stress, leading to parkin translocation, further phosphorylation, and ubiquitination of outer mitochondrial membrane proteins. This ubiquitination is crucial in targeting proteins for degradation or eliminating the whole organelle via mitophagy.
CELLULAR SIGNALLING
(2023)
Article
Cell Biology
Ruixi Li, Zhecheng Wang, Yue Wang, Ruimin Sun, Boyang Zou, Xinyao Tian, Deshun Liu, Xuzi Zhao, Junjun Zhou, Yan Zhao, Jihong Yao
Summary: Damaged mitochondria in liver fibrosis can be eliminated through the mitophagy pathway regulated by SIRT3, PINK1, and NIPSNAP1. SIRT3 deacetylates PINK1 and NIPSNAP1, thereby mediating the mitophagy pathway in liver fibrosis.
JOURNAL OF CELLULAR PHYSIOLOGY
(2023)
Article
Multidisciplinary Sciences
Latika Nagpal, Michael D. Kornberg, Solomon H. Snyder
Summary: This study reveals a key neuroprotective role of IP6K2 in preventing PINK1-mediated mitophagy in the brain. IP6K2 deletion leads to an increase in mitochondrial fission-related proteins and the expression of mitochondrial biogenesis markers. IP6K2 knockout also results in increased glycolysis, potentially as a compensatory mechanism for decreased mitochondrial respiration. IP6K2 exerts its mitoprotective effect through a PINK1-dependent pathway.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2022)
Article
Environmental Sciences
Chao Song, Aiguo Zhang, Man Zhang, Yuzhen Song, Heping Huangfu, Shuangxing Jin, Yanting Sun, Chunhui Zhang, Dongmei Shi, Jundong Wang, Wei Peng, Qin Luo
Summary: This study confirmed that NaF treatment activates mitophagy, and knocking down PINK1 expression attenuates mitophagy and increases mitochondrial impairment, oxidative stress, and apoptosis in NaF-treated HepG2 cells. PINK1 deficiency also exacerbates NaF-induced hepatic mitochondrial injury, oxidative stress, and inflammation in mice livers. Furthermore, Nrf2 signaling is activated by NaF exposure and Nrf2 inhibition blocks the upregulation of PINK1 expression and induction of mitophagy both in vitro and in vivo. In conclusion, Nrf2/PINK1-mediated mitophagy activation offers a hepatoprotective effect against NaF-induced liver injury.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2023)
Article
Chemistry, Multidisciplinary
Zhenqi Liu, Geng Qin, Jie Yang, Wenjie Wang, Wenting Zhang, Boxun Lu, Jinsong Ren, Xiaogang Qu
Summary: Researchers have developed a biochemical method called mito-ATTECs to modulate mitophagy by directly interacting with LC3 on mitochondrial membranes. This approach bypasses the detrimental effects of traditional inducers on mitochondrial membrane integrity and can be used to investigate the physiological roles of mitophagy.
Article
Biochemistry & Molecular Biology
Woo Hyun Shin, Kwang Chul Chung
Summary: Tollip plays a crucial role in PINK1-mediated mitophagy by promoting mitochondrial processing of PINK1 and inhibiting mitochondrial autophagy.
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
Biochemistry & Molecular Biology
Kanika Chandra, M. Swathi, B. Keerthana, Sooraj Gopan, Jyothi Priyanka Ghantasala, Manjunath B. Joshi, Manjunatha Thondamal, Kishore V. L. Parsa
Summary: Adaptability to intracellular or extracellular cues is crucial for maintaining cellular homeostasis. This study reveals the role of PHLPP1 in mitochondrial homeostasis, demonstrating its ability to regulate both fusion and fragmentation of mitochondria under different conditions.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2023)
Article
Endocrinology & Metabolism
Jiongwei Pan, Zaiting Ye, Xiaoping Cai, Hao Zheng, Yiwei Jiang, Xin Wang, Zhuo Cao
Summary: This study investigated the relationship between miR-491-5p and telomerase activity. It was found that miR-491-5p inhibits telomerase reverse transcriptase activity, leading to reduced migration, viability, invasion, and angiogenesis of TIVE cells. Targeting miR-491-5p may regulate the development of tumors by controlling the invasion, migration, and angiogenesis of endothelial cells.
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
(2023)
Article
Biochemistry & Molecular Biology
Li Tao, Wei Zhang, Yaxin Zhang, Mei Zhang, Yueying Zhang, Xing Niu, Qing Zhao, Zhenxing Liu, Yuyin Li, Aipo Diao
Summary: The study showed that caffeine can promote the expression of TERT to extend telomere length and prevent cellular senescence. In animal studies, caffeine also reversed the decline in organ index and improved tissue structure in aging mice. These results suggest that caffeine-containing foods can delay cellular senescence and aging through the expression of TERT.