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The purpose of this study was to examine whether , cultivated in a smart-farming system with LED lamps, could increase exercise capacity in mice. C57BL/6 male mice were orally administered vehicle or water extract (LTE), either 30 or 100 mg/kg, and were subjected to moderate intensity treadmill exercise for 4 weeks. Running distance markedly increased in the LTE group (100 mg/kg) by 80 ± 4% compared to the vehicle group, which was accompanied by a higher proportion of oxidative fibers (6 ± 6% vs. 10 ± 4%). Mitochondrial DNA content and gene expressions related to mitochondrial biogenesis were significantly increased in LTE-supplemented gastrocnemius muscles. At the molecular level, the expression of PGC-1α, a master regulator of fast-to-slow fiber-type transition, was increased downstream of the PKA/CREB signaling pathway. LTE induction of the PKA/CREB signaling pathway was also observed in C2C12 cells, which was effectively suppressed by PKA inhibitors H89 and Rp-cAMP. Altogether, these findings indicate that LTE treatment enhanced endurance exercise capacity via an improvement in mitochondrial biosynthesis and the increases in the formation of oxidative slow-twitch fibers. Future study is warranted to validate the exercise-enhancing effect of LTE in the human.
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http://dx.doi.org/10.3390/nu14193904 | DOI Listing |
RSC Med Chem
August 2025
Department of Biological Science, Birla Institute of Technology and Science, Pilani Hyderabad Campus, Jawahar Nagar, Kapra Mandal, Medchal District Telangana 500078 India
Mitochondrial dysfunction is one of the primary cellular conditions involved in developing Huntington's disease (HD) pathophysiology. The accumulation of mutant huntingtin protein with abnormal PolyQ repeats resulted in the death of striatal neurons with enhanced mitochondrial fragmentation. In search of neuroprotective molecules against HD conditions, we synthesized a set of isoxazole-based small molecules to screen their suitability as beneficial chemicals improving mitochondrial health.
View Article and Find Full Text PDFPhysiol Plant
September 2025
Department of Plant Physiology, Institute of Biology, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Several genes in the mitochondria of angiosperms are interrupted by introns, and their posttranscriptional excision involves numerous nucleus-encoded auxiliary factors. Most of these factors are of eukaryotic origin, among them members of the pentatricopeptide-repeat (PPR) family of RNA-binding proteins. This family divides into the PLS and P classes, with PLS-class proteins typically participating in C-to-U mRNA editing and P-class members contributing to transcript stabilization and intron splicing.
View Article and Find Full Text PDFCurr Biol
September 2025
Institut Necker Enfants Malades, Université Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, F-75015 Paris, France. Electronic address:
Maintaining organelle identity and function relies on endomembrane system specialization and plasticity. A recent study uncovers endolysosomes as an alternative site of melanin production when melanosome biogenesis is impaired, revealing unexpected functional flexibility within the endolysosomal system.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, China-Singapore Belt and Road Joint Laboratory on Infection Research and Drug Development, National Medical Center for Infectious Diseases, Collaborative Innovation Cen
Macrophages play crucial roles in the progression of liver diseases. Increasing studies have shown that mesenchymal stem cells (MSCs) and their extracellular vesicles (MSC-EVs) could reshape the liver immune microenvironment by regulating the function and phenotype of macrophages, thereby exerting a therapeutic effect on liver diseases. Mitochondria, apart from being the central hub of energy metabolism, also finely regulate macrophage-mediated innate immune responses by modulating reactive oxygen species levels, cell polarization, and cell death.
View Article and Find Full Text PDFJCI Insight
September 2025
Division of Cardiovascular Medicine, Department of Medicine.
Aortic valve stenosis is a progressive and increasingly prevalent disease in older adults, with no approved pharmacologic therapies to prevent or slow its progression. Although genetic risk factors have been identified, the contribution of epigenetic regulation remains poorly understood. Here, we demonstrated that histone deacetylase 3 (HDAC3) maintains aortic valve structure by suppressing mitochondrial biogenesis and preserving extracellular matrix integrity in valvular interstitial fibroblasts.
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