mtDNA variability determines spontaneous joint aging damage in a conplastic mouse model
Morena Scotece, Carlos Vaamonde‐García, Ana Victoria Lechuga‐Vieco, Alberto Centeno Cortés, María Concepción Jiménez Gómez, P. Filgueira-Fernández, Ignacio Rego‐Pérez, José Antonio Enrı́quez, Francisco J. Blanco
Abstract
) mice. This study demonstrates that mtDNA genetic manipulation ameliorates joint aging damage in a conplastic mouse model, suggesting that mtDNA variability is a prognostic factor for aging-related osteoarthritis (OA) and that modulation of mitochondrial oxidative phosphorylation (OXPHOS) could be a novel therapeutic target for treating OA associated with aging.
Topics & Concepts
Mitochondrial DNACartilageSenescenceOsteoarthritisDownregulation and upregulationStrain (injury)AutophagyImmunohistochemistryBiologyMitochondrionMouse strainPathologyApoptosisMolecular biologyAndrologyMedicineAnatomyCell biologyImmunologyGeneGeneticsAlternative medicineMitochondrial Function and PathologyOsteoarthritis Treatment and MechanismsMicroRNA in disease regulation