Mitophagy coordination with retrograde transport ensures the integrity of synaptic mitochondria

Han, Sinsuk; Jeong, Yu Young; Sheshadri, Preethi; Cai, Qian

doi:10.1080/15548627.2020.1810919

Cited by 25 publications

(11 citation statements)

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“…These features indicate that prion infection leads to neurological symptoms such as dysfunctions in memory, movement, and cognition [ 3 ]. It has been reported that mitochondrial dysfunction via endoplasmic reticulum (ER) stress, endothelial nitric oxide synthase (eNOS), and oxidative stress, which results in reduced ATP production, increased mitochondrial reactive oxygen species (mtROS) production, and neurodegeneration [ 4 , 5 , 6 , 7 ]. In addition, it has been suggested that aberrant mitochondrial quality control induces neuronal cell death in both in vitro and in vivo models of various neurodegenerative diseases, including Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), Parkinson’s disease (PD), and prion diseases.…”

Section: Introductionmentioning

confidence: 99%

Impairment of Neuronal Mitochondrial Quality Control in Prion-Induced Neurodegeneration

Kim

Jang

et al. 2022

Cells

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Mitochondrial dynamics continually maintain cell survival and bioenergetics through mitochondrial quality control processes (fission, fusion, and mitophagy). Aberrant mitochondrial quality control has been implicated in the pathogenic mechanism of various human diseases, including cancer, cardiac dysfunction, and neurological disorders, such as Alzheimer’s disease, Parkinson’s disease, and prion disease. However, the mitochondrial dysfunction-mediated neuropathological mechanisms in prion disease are still uncertain. Here, we used both in vitro and in vivo scrapie-infected models to investigate the involvement of mitochondrial quality control in prion pathogenesis. We found that scrapie infection led to the induction of mitochondrial reactive oxygen species (mtROS) and the loss of mitochondrial membrane potential (ΔΨm), resulting in enhanced phosphorylation of dynamin-related protein 1 (Drp1) at Ser616 and its subsequent translocation to the mitochondria, which was followed by excessive mitophagy. We also confirmed decreased expression levels of mitochondrial oxidative phosphorylation (OXPHOS) complexes and reduced ATP production by scrapie infection. In addition, scrapie-infection-induced aberrant mitochondrial fission and mitophagy led to increased apoptotic signaling, as evidenced by caspase 3 activation and poly (ADP-ribose) polymerase cleavage. These results suggest that scrapie infection induced mitochondrial dysfunction via impaired mitochondrial quality control processes followed by neuronal cell death, which may have an important role in the neuropathogenesis of prion diseases.

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Section: Introductionmentioning

confidence: 99%

Impairment of Neuronal Mitochondrial Quality Control in Prion-Induced Neurodegeneration

Kim

Jang

et al. 2022

Cells

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“…Mitochondria are intracellular organelles with key roles covering cellular metabolism and are the primary source of adenosine triphosphate (ATP) generated via oxidative phosphorylation (Camara et al, 2010; Perez Ortiz & Swerdlow, 2019). There is extensive literature supporting the role of mitochondrial dysfunction and oxidative damage in the pathogenesis of AD (Gowda et al, 2021; Han, Jeong, Sheshadri, & Cai, 2020; Han, Jeong, Sheshadri, Su, & Cai, 2020; Lin & Beal, 2006; Reddy & Beal, 2008; Swerdlow, 2018). Mitochondrial dysfunction also plays a key role in other neurodegenerative diseases such as Parkinson's disease, multiple sclerosis, Huntington's disease, and amyotrophic lateral sclerosis (ALS) (Camara et al, 2017; Reddy & Reddy, 2011).…”

Section: Introductionmentioning

confidence: 99%

A partial reduction of VDAC1 enhances mitophagy, autophagy, synaptic activities in a transgenic Tau mouse model

Vijayan

Alvir

et al. 2022

Aging Cell

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Alzheimer's disease (AD) is the most common cause of mental dementia in the aged population. AD is characterized by the progressive decline of memory and multiple cognitive functions, and changes in behavior and personality. Recent research has revealed age‐dependent increased levels of VDAC1 in postmortem AD brains and cerebral cortices of APP, APPxPS1, and 3xAD.Tg mice. Further, we found abnormal interaction between VDAC1 and P‐Tau in the AD brains, leading to mitochondrial structural and functional defects. Our current study aimed to understand the impact of a partial reduction of voltage‐dependent anion channel 1 (VDAC1) protein on mitophagy/autophagy, mitochondrial and synaptic activities, and behavior changes in transgenic TAU mice in Alzheimer's disease. To determine if a partial reduction of VDAC1 reduces mitochondrial and synaptic toxicities in transgenic Tau (P301L) mice, we crossed heterozygote VDAC1 knockout (VDAC1+/−) mice with TAU mice and generated double mutant (VDAC1+/−/TAU) mice. We assessed phenotypic behavior, protein levels of mitophagy, autophagy, synaptic, other key proteins, mitochondrial morphology, and dendritic spines in TAU mice relative to double mutant mice. Partial reduction of VDAC1 rescued the TAU‐induced behavioral impairments such as motor coordination and exploratory behavioral changes, and learning and spatial memory impairments in VDAC1+/−/TAU mice. Protein levels of mitophagy, autophagy, and synaptic proteins were significantly increased in double mutant mice compared with TAU mice. In addition, dendritic spines were significantly increased; the mitochondrial number was significantly reduced, and mitochondrial length was increased in double mutant mice. Based on these observations, we conclude that reduced VDAC1 is beneficial in symptomatic‐transgenic TAU mice.

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“…During the second phase (2011–2015), researchers’ attention have mostly been focused on the mitochondrial stress and dynamic network and roles of mitophagy in cancer, heart failure and related diseases ( Egan et al, 2011 ; Dang, 2012 ; Dutta et al, 2013 ; Drew et al, 2014 ; Chourasia et al, 2015 ). During the third phase (2016–2021), researchers mostly attached attention to parkin-mediated mitophagy and its roles in skeletal muscle and inflammation-related diseases ( Akabane et al, 2016 ; Kimura et al, 2017 ; Kravic et al, 2018 ; Lin et al, 2019 ; Han et al, 2020 ; Tran and Reddy, 2021 ). In all, we summarized the main research hotspots below: “mechanism of mitochondrial quality control”, “molecule and signaling pathway in mitophagy” and “mitophagy-related diseases”.…”

Section: Discussionmentioning

confidence: 99%

Bibliometric Insights of Global Research Landscape in Mitophagy

Yin

Yang

et al. 2022

Front. Mol. Biosci.

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Background: Autophagy is a highly regulated and evolutionarily conserved process in eukaryotes which is responsible for protein and organelle degradation. Although this process was described over 60 years ago, the selective autophagy of mitochondria (mitophagy) was recently coined in 2005. Research on the topic of mitophagy has made rapid progress in the past decade, which proposed to play critical roles in human health and disease. This study aimed to visualize the scientific outputs and research trends of mitophagy.Methods: Articles and reviews related to the topic of mitophagy were retrieved from the Web of Science Core Collection on 30 November 2021. Two kinds of software (CiteSpace and VOSviewer) were used to perform a visualized analysis of countries/regions, institutions, authors, journals, references, and keywords.Results: From 2005 to 2021, total 5844 publications on mitophagy were identified for final analysis. The annual number of publications grew yearly over the past 17 years. United States (N = 2025) and Chinese Academy of Sciences is the leading country and institute (N = 112) ranked by the number of publications, respectively. The most productive author was Jun Ren (N = 38) and Derek P. Narendra obtained the most co-cited times (2693 times). The journals with the highest output and the highest co-citation frequency were Autophagy (N = 208) and Journal of Biological Chemistry (co-citation: 17226), respectively. Analyses of references and keywords suggested that “mechanism of mitochondrial quality control”, “molecule and signaling pathway in mitophagy”, and “mitophagy related diseases” were research hotspots, and parkin-mediated mitophagy and its roles in skeletal muscle and inflammation-related diseases may be the frontiers of future research.Conclusion: Although mitophagy research has flourished and attracted attention from all over the world, the regional imbalance in the development of mitophagy research was observed. Our results provided a comprehensive global research landscape of mitophagy from 2005– 2021 from a perspective of bibliometrics, which may serve as a reference for future mitophagy studies.

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Mitophagy coordination with retrograde transport ensures the integrity of synaptic mitochondria

Cited by 25 publications

References 0 publications

Impairment of Neuronal Mitochondrial Quality Control in Prion-Induced Neurodegeneration

Impairment of Neuronal Mitochondrial Quality Control in Prion-Induced Neurodegeneration

A partial reduction of VDAC1 enhances mitophagy, autophagy, synaptic activities in a transgenic Tau mouse model

Bibliometric Insights of Global Research Landscape in Mitophagy

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