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Mitochondria Express Functional Signaling Ligand-Binding Receptors that Regulate their Biological Responses - the Novel Role of Mitochondria as Stress-Response Sentinels.
Stem Cell Rev Rep
January 2025
Department of Regenerative Medicine, Warsaw Medical University, Warsaw, Poland.
Evidence accumulated mitochondria, as the "powerplants of the cell," express several functional receptors for external ligands that modify their function and regulate cell biology. This review sheds new light on the role of these organelles in sensing external stimuli to facilitate energy production for cellular needs. This is possible because mitochondria express some receptors on their membranes that are responsible for their autonomous responses.
View Article and Find Full Text PDFDefective Cystic Fibrosis Transmembrane Conductance Regulator Accelerates Skeletal Muscle Aging by Impairing Autophagy/Myogenesis.
J Cachexia Sarcopenia Muscle
February 2025
Musculoskeletal Research Laboratory, Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
Background: Regenerative capacity of skeletal muscles decreases with age. Deficiency in cystic fibrosis transmembrane conductance regulator (CFTR) is associated with skeletal muscle weakness as well as epithelial cell senescence. However, whether and how CFTR plays a role in skeletal muscle regeneration and aging were unclear.
View Article and Find Full Text PDFOsteoblast-Derived Mitochondria Formulated with Cationic Liposome Guide Mesenchymal Stem Cells into Osteogenic Differentiation.
Adv Sci (Weinh)
January 2025
School of Bioconvergence, CHA University, 6F, CHA Biocomplex, Sampyeong-Dong, Bundang-gu, Seongnam-si, 13488, Republic of Korea.
While mitochondria are known to be essential for intracellular energy production and overall function, emerging evidence highlights their role in influencing cell behavior through mitochondrial transfer. This phenomenon provides a potential basis for the development of treatment strategies for tissue damage and degeneration. This study aims to evaluate whether mitochondria isolated from osteoblasts can promote osteogenic differentiation in mesenchymal stem cells (MSCs).
View Article and Find Full Text PDFMitochondrial DNA copy number alterations: Key players in the complexity of glioblastoma (Review).
Mol Med Rep
March 2025
Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan 16150, Malaysia.
Renowned as a highly invasive and lethal tumor derived from neural stem cells in the central nervous system, glioblastoma (GBM) exhibits substantial histopathological variation and genomic complexity, which drive its rapid progression and therapeutic resistance. Alterations in mitochondrial DNA (mtDNA) copy number (CN) serve a crucial role in GBM development and progression, affecting various aspects of tumor biology, including energy production, oxidative stress regulation and cellular adaptability. Fluctuations in mtDNA levels, whether elevated or diminished, can impair mitochondrial function, potentially disrupting oxidative phosphorylation and amplifying reactive oxygen species generation, thereby fueling tumor growth and influencing treatment responses.
View Article and Find Full Text PDFAn extracellular vesicle based hypothesis for the genesis of the polycystic kidney diseases.
Extracell Vesicle
December 2024
The Jared Grantham Kidney Institute at the University of Kansas Medical Center, Department of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Autosomal dominant polycystic kidney (ADPKD) disease is the commonest genetic cause of kidney failure (affecting 1:800 individuals) and is due to heterozygous germline mutations in either of two genes, and . Homozygous germline mutations in are responsible for autosomal recessive polycystic kidney (ARPKD) disease a rare (1:20,000) but severe neonatal disease. The products of these three genes, (polycystin-1 (PC1 4302(3)aa)), (polycystin-2 (PC2 968aa)) and (fibrocystin (4074aa)) are all present on extracellular vesicles (EVs) termed, PKD-exosome-like vesicles (PKD-ELVs).
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