Article
Biochemistry & Molecular Biology
Catherine Kim, Meredith Juncker, Ryan Reed, Arthur Haas, Jessie Guidry, Michael Matunis, Wei-Chih Yang, Joshua Schwartzenburg, Shyamal Desai
Summary: In cells treated with mitochondrial stressors, SUMOylation of Mfn1/2 facilitates the aggregation of damaged mitochondria at the perinuclear region, potentially through acting as a molecular glue to interact with other proteins.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2021)
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)
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)
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
Neurosciences
Laura Scott, Senthilkumar S. Karuppagounder, Stewart Neifert, Bong Gu Kang, Hu Wang, Valina L. Dawson, Ted M. Dawson
Summary: In this study, a transgenic model was generated to examine the impact of Parkin loss on mitochondrial function in PolgAD257A/D257A mice. Surprisingly, no dopaminergic neurodegeneration or nigral-striatal neurobehavioral deficits were observed in these mice. These findings suggest a lack of synergism between Parkin loss and mitochondrial dysfunction in this mouse model of mitochondrial deficits.
JOURNAL OF NEUROSCIENCE
(2022)
Article
Chemistry, Multidisciplinary
Ziwen Jiang, Yu-Hsuan Kuo, Michelle R. Arkin
Summary: Autophagy is a crucial process for the degradation of large cellular contents, and impaired autophagy can lead to pathological aggregation. This study developed a novel method for targeted degradation of protein aggregates and organelles in mammalian cells.
JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
(2023)
Review
Cell Biology
Rachel Y. Diao, Asa B. Gustafsson
Summary: Mitophagy is a vital quality control pathway in the heart that removes unwanted or dysfunctional mitochondria, preventing damage to proteins and DNA and suppressing inflammation and cell death. Impairments in mitophagy are associated with various diseases.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Nadezda Apostolova, Teresa Vezza, Jordi Muntane, Milagros Rocha, Victor M. Victor
Summary: Type 2 diabetes mellitus is closely linked to oxidative stress, mitochondrial dysfunction, and alterations in autophagy and mitophagy. Despite progress in understanding the molecular events associated with these processes, effective therapeutic strategies targeting these mechanisms are yet to be implemented.
ANTIOXIDANTS & REDOX SIGNALING
(2023)
Article
Cell Biology
Sylwia M. Kacprzak, Olivier Van Aken
Summary: This study reveals that carbon starvation induced by dark-incubation, natural senescence, and specific mitochondrial stresses are key triggers of mitophagy in plants.
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.
Editorial Material
Cell Biology
Tomoyuki Fukuda, Kentaro Furukawa, Tatsuro Maruyama, Nobuo N. Noda, Tomotake Kanki
Summary: Mitophagy is a selective form of autophagy that targets dysfunctional or superfluous mitochondria for degradation. Our recent study has identified Atg44 as a mitochondrial fission factor that generates mitochondrial fragments suitable for phagophore engulfment. We propose the term mitofissin to refer to Atg44 and its homologous proteins that might participate in diverse cellular processes.
Article
Biochemistry & Molecular Biology
Guiomar Rodriguez-Perinan, Ana de la Encarnacion, Fermin Moreno, Adolfo Lopez de Munain, Ana Martinez, Angeles Martin-Requero, Carolina Alquezar, Fernando Bartolome
Summary: LOF mutations in GRN gene cause FTLD-TDP, and mitochondrial dysfunction is involved in the pathogenesis of PGRN deficiency-associated FTLD-TDP. PGRN deficiency induces mitochondrial depolarization, elevated ROS production, and reduced ATP levels. The accumulation of damaged mitochondria and autophagy dysfunction were observed in PGRN-deficient cells, which can be rescued by CK-1 delta inhibitors.
Editorial Material
Cell Biology
Samuel A. Killackey, Yuntian Bi, Dana J. Philpott, Damien Arnoult, Stephen E. Girardin
Summary: Mitochondrial protein import stress has been identified as a potential common trigger for mitophagy, offering new avenues for therapeutic exploration and mechanistic insights.
Article
Chemistry, Medicinal
Runjie Sun, Jiang Liu, Manya Yu, Mengting Xia, Yanyu Zhang, Xiaoqi Sun, Yunsheng Xu, Xing Cui
Summary: This study confirmed the therapeutic effect of paeoniflorin on Bortezomib-induced peripheral neuropathy (BiPN) by reducing IL6 levels and regulating PARKIN-mediated mitochondrial autophagy and mitochondrial damage.
DRUG DESIGN DEVELOPMENT AND THERAPY
(2022)
Review
Cell Biology
Serra Ozgen, Judith Krigman, Ruohan Zhang, Nuo Sun
Summary: Mitochondria play a crucial role in the function and vitality of the neurological system, particularly in regulating neural pathways' homeostasis and neurogenesis. Understanding the molecular intricacies of mitochondria in neurogenesis and neuron vitality is important in finding potential pharmaceutical targets for neurodegenerative diseases.
NEURAL REGENERATION RESEARCH
(2022)