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PEX1 remains functional in peroxisome biogenesis but is rapidly degraded by the proteasome.
bioRxiv
December 2024
Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, Santa Barbara, CA 93106, USA.
The PEX1/PEX6 AAA-ATPase is required for the biogenesis and maintenance of peroxisomes. Mutations in and disrupt peroxisomal matrix protein import and are the leading cause of Peroxisome Biogenesis Disorders (PBDs). The most common disease-causing mutation in PEX1 is the PEX1 allele, which results in a reduction of peroxisomal protein import.
View Article and Find Full Text PDFMuscle PGC-1α Overexpression Drives Metabolite Secretion Boosting Subcutaneous Adipocyte Browning.
J Cell Physiol
December 2024
Department of Clinical Medicine and Surgery, University of Naples "Federico II", Naples, Italy.
Muscle and adipose tissue (AT) are in mutual interaction through the integration of endocrine and biochemical signals, thus regulating whole-body function and physiology. Besides a traditional view of endocrine relationships that imply the release of cytokines and growth factors, it is becoming increasingly clear that a metabolic network involving metabolites as signal molecules also exists between the two tissues. By elevating the number and functionality of mitochondria, a key role in muscle metabolism is played by the master regulator of mitochondrial biogenesis peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α), that induces a fiber type shift from glycolytic to oxidative myofibers.
View Article and Find Full Text PDFSulforaphane treatment mimics contractile activity-induced mitochondrial adaptations in muscle myotubes.
Am J Physiol Cell Physiol
December 2024
Muscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, Ontario, M3J 1P3, Canada.
Mitochondria are metabolic hubs that govern skeletal muscle health. While exercise has been established as a powerful inducer of quality control processes that ultimately enhance mitochondrial function, there are currently limited pharmaceutical interventions available that emulate exercise-induced mitochondrial adaptations. To investigate a novel candidate for this role, we examined Sulforaphane (SFN), a naturally occurring compound found in cruciferous vegetables.
View Article and Find Full Text PDFPhosphocreatine-mediated enhancement of mitochondrial function for accelerated healing of diabetic foot ulcers through the PGC-1α-NRF-1 signaling pathway.
Tissue Cell
December 2024
Collage of Pharmacology, Dalian Medical University, 9 West Section, South Road of Lushun, Dalian 116044, China. Electronic address:
Diabetic foot ulcers (DFUs) pose a significant clinical challenge due to their slow healing and high risk of complications, which severely affect patient quality of life. Central to the delayed healing observed in DFUs is mitochondrial dysfunction, a critical factor impairing cellular repair processes. Phosphocreatine (PCr), a vital molecule involved in cellular energy buffering and ATP regeneration, has recently emerged as a promising therapeutic candidate for ameliorating mitochondrial dysfunction and enhancing tissue repair.
View Article and Find Full Text PDFPeroxisomes are underappreciated organelles hijacked by viruses.
Trends Cell Biol
December 2024
University of Montpellier, CNRS, Institut de Recherche en Infectiologie de Montpellier (IRIM), Montpellier, France. Electronic address:
Peroxisomes are cellular organelles that are crucial for metabolism, stress responses, and healthy aging. They have recently come to be considered as important mediators of the immune response during viral infections. Consequently, various viruses target peroxisomes for the purpose of hijacking either their biogenesis or their functions, as a means of replicating efficiently, making this a compelling research area.
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