4.7 Review

Control of mitochondrial dynamics and apoptotic pathways by peroxisomes

Journal

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2022.938177

Keywords

peroxisomes; mitochondria; fission-fusion; apoptosis; organelle interaction; Zellwegersyndrome; tethering

Funding

  1. Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan
  2. Core Research for Evolutionary Science and Technology of the Japan Science and Technology Agency
  3. Japan Society for the Promotion of Science (JSPS)
  4. Global Centers of Excellence Program (Integrative Life Science Based on the Study of Biosignaling Mechanisms) of MEXT
  5. Graduate Program for Leaders in Life Innovation, The University of Tokyo Life Innovation Leading Graduate School, of MEXT
  6. JSPS KAKENHI [JP26116007, JP17H03675, JP16H05773, JP16H06280, JP18J14098]

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Peroxisomes are organelles that play a role in various metabolic pathways. Their biogenesis is controlled by a group of proteins, and mutations in these proteins can cause metabolic disorders. Recent research has shown that peroxisomes are involved in regulating cell apoptosis and fusion processes, and disruption of these processes may be related to the pathogenesis of specific diseases.
Peroxisomes are organelles containing different enzymes that catalyze various metabolic pathways such as beta-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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