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      Control of mitochondrial dynamics and apoptotic pathways by peroxisomes

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          Abstract

          Peroxisomes are organelles containing different enzymes that catalyze various metabolic pathways such as β-oxidation of very long-chain fatty acids and synthesis of plasmalogens. Peroxisome biogenesis is controlled by a family of proteins called peroxins, which are required for peroxisomal membrane formation, matrix protein transport, and division. Mutations of peroxins cause metabolic disorders called peroxisomal biogenesis disorders, among which Zellweger syndrome (ZS) is the most severe. Although patients with ZS exhibit severe pathology in multiple organs such as the liver, kidney, brain, muscle, and bone, the pathogenesis remains largely unknown. Recent findings indicate that peroxisomes regulate intrinsic apoptotic pathways and upstream fission-fusion processes, disruption of which causes multiple organ dysfunctions reminiscent of ZS. In this review, we summarize recent findings about peroxisome-mediated regulation of mitochondrial morphology and its possible relationship with the pathogenesis of ZS.

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          Most cited references76

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          Role of reactive oxygen species (ROS) in apoptosis induction.

          Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.
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            The cell biology of mitochondrial membrane dynamics

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              ER tubules mark sites of mitochondrial division.

              Mitochondrial structure and distribution are regulated by division and fusion events. Mitochondrial division is regulated by Dnm1/Drp1, a dynamin-related protein that forms helices around mitochondria to mediate fission. Little is known about what determines sites of mitochondrial fission within the mitochondrial network. The endoplasmic reticulum (ER) and mitochondria exhibit tightly coupled dynamics and have extensive contacts. We tested whether ER plays a role in mitochondrial division. We found that mitochondrial division occurred at positions where ER tubules contacted mitochondria and mediated constriction before Drp1 recruitment. Thus, ER tubules may play an active role in defining the position of mitochondrial division sites.
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                Author and article information

                Contributors
                Journal
                Front Cell Dev Biol
                Front Cell Dev Biol
                Front. Cell Dev. Biol.
                Frontiers in Cell and Developmental Biology
                Frontiers Media S.A.
                2296-634X
                09 September 2022
                2022
                : 10
                : 938177
                Affiliations
                [1] 1 Graduate School of Pharmaceutical Sciences , The University of Tokyo , Tokyo, Japan
                [2] 2 Laboratory of Molecular Cell Biology , Institute for Genetic Medicine , Hokkaido University , Sapporo, Hokkaido, Japan
                Author notes

                Edited by: Amr Kataya, University of Calgary, Canada

                Reviewed by: Andrew Simmonds, University of Alberta, Canada

                Markus Kunze, Medical University of Vienna, Austria

                *Correspondence: Tomohiko Okazaki, okazaki@ 123456igm.hokudai.ac.jp

                This article was submitted to Signaling, a section of the journal Frontiers in Cell and Developmental Biology

                Article
                938177
                10.3389/fcell.2022.938177
                9500405
                36158224
                e509a4ee-5c98-42c4-8a10-1d5787eefa5a
                Copyright © 2022 Jiang and Okazaki.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 07 May 2022
                : 26 August 2022
                Categories
                Cell and Developmental Biology
                Review

                peroxisomes,mitochondria,fission-fusion,apoptosis,organelle interaction,zellweger syndrome,tethering

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