Article
Biochemistry & Molecular Biology
Taiki Baba, Susumu Tanimura, Ayane Yamaguchi, Koichiro Horikawa, Masashi Yokozeki, Saki Hachiya, Shun-Ichiro Iemura, Tohru Natsume, Noriyuki Matsuda, Kohsuke Takeda
Summary: PGAM5 is a protein phosphatase located in the inner mitochondrial membrane, which is cleaved and released into the nucleus upon mitochondrial dysfunction. It interacts with nuclear protein SRm160, dephosphorylates it, and regulates phosphorylation of other SR proteins during mitophagy, potentially coordinating cellular responses to mitochondrial stress at the post-transcriptional and pretranslational levels.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
(2021)
Review
Pharmacology & Pharmacy
Alexander V. Blagov, Andrey G. Goncharov, Olga O. Babich, Viktoriya V. Larina, Alexander N. Orekhov, Alexandra A. Melnichenko
Summary: This review discusses the use of mitophagy activators as a class of drug compounds for the treatment of Parkinson's disease, and explores the impact of mutations in Pink1 and Parkin enzymes on mitophagy.
Article
Cell Biology
Jessica Elswood, Scott J. Pearson, H. Ross Payne, Rola Barhoumi, Monique Rijnkels, Weston W. Porter
Summary: Through studying the differentiation and metabolism of mammary epithelial cells, it was found that mitophagy occurs selectively during the differentiation process. Inhibiting autophagy impairs cell differentiation, while the PRKN protein is necessary for cell differentiation.
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
Cell Biology
Weili Li, Xiaoping Wang, Tianhua Liu, Qian Zhang, Jing Cao, Yanyan Jiang, Qianbin Sun, Chun Li, Wei Wang, Yong Wang
Summary: Doxorubicin is an effective chemotherapeutic agent, but its clinical use is limited due to the severe risk of cardiotoxicity. This study finds that harpagoside has significant cardioprotective effects in DICT mouse and rat cardiomyocytes by targeting the interaction between p53 and Parkin to restore mitophagy.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
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.
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
Cell Biology
Matthew Kim, Azadeh Nikouee, Yuxiao Sun, Qing-Jun Zhang, Zhi-Ping Liu, Qun Sophia Zang
Summary: The study suggests that the Parkin/PINK1 mitophagy pathway is involved in the regulation of cardiac mitochondria-associated membranes (MAMs) during endotoxemia. However, the W402A point mutation is not sufficient to alleviate endotoxemia-induced cardiomyopathy.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Isshin Shiiba, Keisuke Takeda, Shun Nagashima, Naoki Ito, Takeshi Tokuyama, Shun-Ichi Yamashita, Tomotake Kanki, Toru Komatsu, Yasuteru Urano, Yuuta Fujikawa, Ryoko Inatome, Shigeru Yanagi
Summary: MITOL regulates Parkin-mediated cell death by promoting ubiquitination of Parkin at lysine 220 residue, leading to its proteasomal degradation and controlling mitophagy. Deletion of MITOL results in accumulation of active phosphorylated Parkin in the ER, causing FKBP38 degradation and increased cell death.
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
Roberto Iorio, Giuseppe Celenza, Sabrina Petricca
Summary: Mitochondria are critical organelles for cellular energy balance and cell death. Mitophagy, the selective removal of dysfunctional mitochondria by autophagy, plays important roles in maintaining mitochondrial health. Both impaired and excessive mitophagy are involved in various ageing-associated diseases. Recent advances have explored the molecular mechanisms and signaling pathways that regulate mitophagy, including the early role and spatial specificity of the AMPK/ULK1 axis.
Review
Cardiac & Cardiovascular Systems
Yanze Wu, Ting Jiang, Jinghai Hua, Zhiping Xiong, Kai Dai, Hui Chen, Lei Li, Jingtian Peng, Xiaoping Peng, Zeqi Zheng, Wenjun Xiong
Summary: Cardiovascular disease is one of the leading causes of death and illness. Mitochondrial dysfunction and excessive production of ROS can lead to oxidative damage and contribute to cardiovascular diseases. The role of PINK1/Parkin-mediated mitophagy in maintaining cardiac homeostasis and regulating metabolic transition is significant. Understanding and modulating PINK1/Parkin-mediated mitophagy may have therapeutic implications for cardiovascular diseases.
INTERNATIONAL JOURNAL OF CARDIOLOGY
(2022)
Editorial Material
Cell Biology
Yumiko Oshima, Nicolas Verhoeven, Etienne Cartier, Mariusz Karbowski
Summary: Mitochondrial membrane dynamics, UPS activity, and mitochondrial fission play critical roles in maintaining mitochondrial function. Under acute reduction of mitochondrial translation fidelity, mosaic distribution of mitochondria was observed within a single cell, with some showing enriched population and some reduced levels of specific proteins in the intermembrane space. In the absence of PRKN activity, mosaic mitochondria formation is followed by OMM severing, IMM protein ubiquitination, and formation of mito-autophagosomes.
Review
Cell Biology
Pernille Y. O. Nielsen, Justyna Okarmus, Morten Meyer
Summary: Parkinson's disease is associated with mitochondrial dysfunction, oxidative stress, defects in mitophagy, and oc-synuclein-positive inclusions. The deubiquitinating enzymes (DUBs) play a role in regulating mitophagy and oc-synuclein aggregation. This paper describes the DUBs associated with Parkinson's disease and their potential as therapeutic targets.
Article
Biochemistry & Molecular Biology
Fumika Koyano, Koji Yamano, Hidetaka Kosako, Yoko Kimura, Mayumi Kimura, Yukio Fujiki, Keiji Tanaka, Noriyuki Matsuda
Article
Chemistry, Multidisciplinary
Nana Nakada-Motokawa, Taiga Miyazaki, Satoshi Mizuta, Yoshimasa Tanaka, Tatsuro Hirayama, Takahiro Takazono, Tomomi Saijo, Kazuko Yamamoto, Yoshifumi Imamura, Koichi Izumikawa, Katsunori Yanagihara, Koichi Makimura, Kohsuke Takeda, Shigeru Kohno, Hiroshi Mukae
Review
Neurosciences
Noriyuki Matsuda, Koji Yamano
NEUROSCIENCE RESEARCH
(2020)
Article
Cell Biology
Koji Yamano, Reika Kikuchi, Waka Kojima, Ryota Hayashida, Fumika Koyano, Junko Kawawaki, Takuji Shoda, Yosuke Demizu, Mikihiko Naito, Keiji Tanaka, Noriyuki Matsuda
JOURNAL OF CELL BIOLOGY
(2020)
Article
Cell Biology
Shota Nakamura, Ritsuko Masuyama, Kosuke Sakai, Karin Fukuda, Kohsuke Takeda, Susumu Tanimura
Review
Biochemistry & Molecular Biology
Mashun Onishi, Koji Yamano, Miyuki Sato, Noriyuki Matsuda, Koji Okamoto
Summary: Mitophagy is a fundamental cellular mechanism for degrading mitochondria, regulated by specific receptors or ubiquitin molecules. Its dysfunction is associated with various pathological conditions, highlighting its biological significance in maintaining cellular homeostasis.
Article
Cell Biology
Waka Kojima, Koji Yamano, Hidetaka Kosako, Kenichiro Imai, Reika Kikuchi, Keiji Tanaka, Noriyuki Matsuda
Summary: Macroautophagy/autophagy is a complex intracellular degradation process with many regulatory factors. This study identified BCAS3 and C16orf70 as novel proteins associated with the autophagosome formation site and demonstrated their regulatory roles in autophagic activity. The BCAS3-C16orf70 complex affects the recruitment of core autophagy proteins to the phagophore assembly site.
Article
Oncology
Makoto Fujimoto, Miki Kamiyama, Kosuke Fuse, Hiroki Ryuno, Takeru Odawara, Natsuki Furukawa, Yasuhiro Yoshimatsu, Tetsuro Watabe, Michaela Prchal-Murphy, Veronika Sexl, Hideaki Tahara, Yoshihiro Hayakawa, Takehiro Sato, Kohsuke Takeda, Isao Naguro, Hidenori Ichijo
Summary: The study demonstrates that ASK1 deficiency promotes NK cell-mediated intravascular tumor cell clearance and upregulates immune response-related genes, including IFN gamma, to enhance the anti-metastatic phenotypes. NK cells are required for these anti-metastatic phenotypes.
Article
Biochemistry & Molecular Biology
Tianli Zhang, Hiroyasu Tsutsuki, Waliul Islam, Katsuhiko Ono, Kohsuke Takeda, Takaaki Akaike, Tomohiro Sawa
Summary: ATP exposure leads to a sharp decrease in glutathione (GSH) levels in macrophages, triggering NLRP3 inflammasome activation. Exogenous addition of GSH or GSSG can inhibit GSH efflux and attenuate NLRP3 inflammasome activation. This finding may contribute to the development of novel therapeutic strategies for NLRP3 inflammasome-associated disorders.
Article
Biochemistry & Molecular Biology
Taiki Baba, Susumu Tanimura, Ayane Yamaguchi, Koichiro Horikawa, Masashi Yokozeki, Saki Hachiya, Shun-Ichiro Iemura, Tohru Natsume, Noriyuki Matsuda, Kohsuke Takeda
Summary: PGAM5 is a protein phosphatase located in the inner mitochondrial membrane, which is cleaved and released into the nucleus upon mitochondrial dysfunction. It interacts with nuclear protein SRm160, dephosphorylates it, and regulates phosphorylation of other SR proteins during mitophagy, potentially coordinating cellular responses to mitochondrial stress at the post-transcriptional and pretranslational levels.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
(2021)
Article
Multidisciplinary Sciences
Yukiko Yoshida, Makoto Asahina, Arisa Murakami, Junko Kawawaki, Meari Yoshida, Reiko Fujinawa, Kazuhiro Iwai, Ryuichi Tozawa, Noriyuki Matsuda, Keiji Tanaka, Tadashi Suzuki
Summary: Mutation in the NGLY1 gene leads to a recessive disorder in humans. Findings in this study suggest that dysfunction of the proteasome caused by accumulation of N-glycoproteins, particularly NRF1 ubiquitinated by SCFFBS2, contributes to the pathogenesis resulting from NGLY1 deficiency.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Cell Biology
Bruno Barros Queliconi, Waka Kojima, Mayumi Kimura, Kenichiro Imai, Chisato Udagawa, Chie Motono, Takatsugu Hirokawa, Shinya Tashiro, Jose M. M. Caaveiro, Kouhei Tsumoto, Koji Yamano, Keiji Tanaka, Noriyuki Matsuda
Summary: The study reveals that pathogenic mutations in the PARK7 gene encoding DJ-1 protein lead to its import into the mitochondrial matrix for degradation due to protein unfolding. Increasing structural stability of these mutants restores cytosolic localization, and a reduction in structural stability exposes a mitochondrial-targeting signal for DJ-1 import into the mitochondria.
JOURNAL OF CELL SCIENCE
(2021)