Is osteoarthritis a mitochondrial disease? What is the evidence : Current Opinion in Rheumatology

Secondary Logo

Journal Logo

OSTEOARTHRITIS: Edited by Mukundan Attur

Is osteoarthritis a mitochondrial disease? What is the evidence

Fernández-Moreno, Mercedes; Rego-Pérez, Ignacio; Blanco, Francisco J.

Author Information
Current Opinion in Rheumatology 34(1):p 46-53, January 2022. | DOI: 10.1097/BOR.0000000000000855


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


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.

Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.

You can read the full text of this article if you:

Access through Ovid