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Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 9 months-old mice

ABSTRACT: We generated a muscle-specific Pex5 KO mouse to investigate the consequences of peroxisomal dysfunction on muscle homeostasis. Our study reveals that peroxisomal impairment triggers early alterations in skeletal muscle lipid and amino acid metabolism and disrupts the physical interaction between peroxisomes and mitochondria, resulting in reduction of muscle force and exercise performance. Over time, these disruptions lead to metabolic changes that affect mitochondrial content, and function anticipating the development of age-related muscle dysfunction.

ORGANISM(S): Mus musculus

PROVIDER: GSE263104 | GEO | 2025/09/16

REPOSITORIES: GEO

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Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 3 months-old mice

Project description:We generated a muscle-specific Pex5 KO mouse to investigate the consequences of peroxisomal dysfunction on muscle homeostasis. Our study reveals that peroxisomal impairment triggers early alterations in skeletal muscle lipid and amino acid metabolism and disrupts the physical interaction between peroxisomes and mitochondria, resulting in reduction of muscle force and exercise performance. Over time, these disruptions lead to metabolic changes that affect mitochondrial content, and function anticipating the development of age-related muscle dysfunction.

2025-09-16 | GSE263103 | GEO

Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 18 months-old mice

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Proteomic analysis of peroxisome-associated PEX5 mutants in Xenopus egg extract.

Project description:This project sought to identify the features in PEX5 required for interaction with the peroxisomal PEX2-PEX10-PEX12 ubiquitin ligase complex. Peroxisomes equilibrated with different PEX5 mutants (i.e., C11A, AH1, AH2) were purified from Xenopus egg extract, solubilized in digitonin, and PEX5-associated material was immunoprecipitated via a C-terminal FLAG tag. PEX5 without a FLAG tag was used as a negative control. PEX5-interacting peroxins were identified by LC-MS/MS at the Taplin Mass Spectrometry Facility at Harvard Medical School.

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White adipose tissue from aP2-Pex5 knockout and control mice

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Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle

Project description:Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle

| PRJNA1095854 | ENA

Loss of pex5 sensitizes zebrafish to fasting due to deregulated mitochondria, mTOR, and autophagy

Project description:Animal models have been utilized to understand the pathogenesis of Zellweger spectrum disorders (ZSD), but the link between the clinical manifestations and molecular pathways has not yet been clearly established. We generated a peroxin 5 homozygous mutant zebrafish (pex5-/-) to gain insight into the molecular pathogenesis of peroxisome dysfunction. pex5-/- displays hallmarks of ZSD in humans and die within one month after birth. Fasting rapidly depletes the liver lipids and glycogen in pex5-/- and expedites their mortality. Mechanistically, abnormal mitochondrial activity and mechanistic target of rapamycin (mTOR) signaling act together to induce metabolic alterations to deplete the hepatic nutrients and accumulate the damaged mitochondria. Accordingly, the use of chemical interventions blocking either the mitochondrial activities or the mechanistic target of rapamycin complex 1 or a combination of both improves the metabolic imbalance shown in the fasted pex5-/- livers and extends the survival of the animals. Furthermore, the use of an autophagy activator also effectively ameliorated the early mortality of the fasted pex5-/-. These results suggest that fasting may be detrimental to patients with peroxisome dysfunction and that modulating the mitochondria, mTOR, or autophagy activities may provide a therapeutic option to alleviate the symptoms of peroxisomal diseases associated with metabolic dysfunction.

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Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 18 months-old mice

Project description:Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 18 months-old mice

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Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 9 months-old mice

Project description:Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 9 months-old mice

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Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 3 months-old mice

Project description:Effect of muscle-specific Pex5 depletion on gene expression in gastrocnemius muscle in 3 months-old mice

| PRJNA1095859 | ENA

PEX5 integrates p38 MAPK signaling pathway and taurine metabolism to regulate cellular senescence in lung fibroblasts

Project description:Chronic lung diseases significantly impact the aging population globally, but their etiology is largely unknown, and the therapeutic options are minimal. Cellular senescence has been increasingly recognized as an essential driving mechanism for chronic lung diseases. Remodeling in subcellular compartments is commonly observed in senescent cells, which reciprocally regulates the senescent progression. Roles of peroxisomes in cellular senescence have been documented, but the molecular mechanisms for this regulation remain poorly understood. Here, we showed that the peroxisome pathway and the shuttling receptor PEX5 are downregulated during replicative and oxidative senescence in human fetal lung fibroblast 1 (HFL-1) cells. PEX5 knockdown can induce senescence via transcriptional suppression of LAMP1 and autophagic flux. Further study revealed that activation of the p38 MAPK signaling pathway and subsequent nuclear localization of transcription factor EB (TFEB) are the significant retrograde signals contributing to the PEX5 regulation of cellular senescence. Metabolomics analysis identified a substantial increase in taurine levels in cells with PEX5 overexpression. Reciprocally, treatment of cells with taurine enhanced PEX5 levels in the senescent HFL-1 cells and the lungs of aged mice and alleviated senescence, suggesting the presence of a taurine-dependent response in PEX5 regulation of cellular senescence. Collectively, our findings provided new insights into the peroxisomal regulation of cellular senescence by integrating the p38 MAPK retrograde signaling pathway and taurine metabolism, which may help develop anti-aging strategies to treat chronic lung diseases.

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