Is osteoarthritis a mitochondrial disease? What is the evidence. Issue 1 (January 2022)

• Record Type: Journal Article
• Authors: Fernández-Moreno, Mercedes; Rego-Pérez, Ignacio; Blanco, Francisco J.
• Is Part Of: Current opinion in rheumatology. Volume 34:Issue 1(2022)
• Publication Date: 2022-01
• Subjects: apoptosis -- cartilage -- mitochondria -- mtDNA -- osteoarthritis; Rheumatology -- Periodicals; Arthritis -- Periodicals; Review Literature -- Periodicals; Rheumatic Diseases -- Periodicals; 616.723
• DOI: 10.1097/BOR.0000000000000855
• Languages: English
• ISSNs: 1040-8711

Abstract

Abstract : Propose of review: To summarize the evidence that suggests that osteoarthritis (OA) is a mitochondrial disease. Recent findings: Mitochondrial dysfunction together with mtDNA damage could contribute to cartilage degradation via several processes such as: (1) increased apoptosis; (2) decreased autophagy; (3) enhanced inflammatory response; (4) telomere shortening and increased senescence chondrocytes; (5) decreased mitochondrial biogenesis and mitophagy; (6) increased cartilage catabolism; (7) increased mitochondrial fusion leading to further reactive oxygen species production; and (8) impaired metabolic flexibility Summary: Mitochondria play an important role in some events involved in the pathogenesis of OA, such as energy production, the generation of reactive oxygen and nitrogen species, apoptosis, authophagy, senescence and inflammation. The regulation of these processes in the cartilage is at least partially controlled by retrograde regulation from mitochondria and mitochondrial genetic variation. Retrograde regulation through mitochondrial haplogroups exerts a signaling control over the nuclear epigenome, which leads to the modulation of nuclear genes, cellular functions and development of OA. All these data suggest that OA could be considered a mitochondrial disease as well as other complex chronic disease as cancer, cardiovascular and neurologic diseases.