Specific premature epigenetic aging of cartilage in osteoarthritis

Osteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have...

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Detalles Bibliográficos
Autores: Vidal Bralo, L, López Golán, Y, Mera Varela, A, Rego Pérez, Ignacio, Horvath, S, Zhang, Y, Real Bolt, Álvaro del|||0000-0002-1057-461X, Zhai, G, Blanco, FJ, Riancho Moral, José Antonio|||0000-0003-0691-8755, Gómez Reino, JJ, González, A
Tipo de recurso: artículo
Fecha de publicación:2016
País:España
Institución:Universidad de Cantabria (UC)
Repositorio:UCrea Repositorio Abierto de la Universidad de Cantabria
Idioma:inglés
OAI Identifier:oai:repositorio.unican.es:10902/9265
Acceso en línea:http://hdl.handle.net/10902/9265
Access Level:acceso abierto
Palabra clave:Osteoarthritis
Biological age
Epigenetics
DNA methylation
Telomere length shortening
Descripción
Sumario:Osteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have explored epigenetic aging in OA at the local (cartilage and bone) and systemic (blood) levels. Two DNA methylation age‐measures (DmAM) were used: the multi‐tissue age estimator for cartilage and bone; and a blood‐specific biomarker for blood. Differences in DmAM between OA patients and controls showed an accelerated aging of 3.7 years in articular cartilage (95 % CI = 1.1 to 6.3, P = 0.008) of OA patients. By contrast, no difference in epigenetic aging was observed in bone (0.04 years; 95 % CI = ‐1.8 to 1.9, P = 0.3) and in blood (‐0.6 years; 95 % CI = ‐1.5 to 0.3, P = 0.2) between OA patients and controls. Therefore, premature epigenetic aging according to DNA methylation changes was specific of OA cartilage, adding further evidence and insight on premature aging of cartilage as a component of OA pathogenesis that reflects damage and vulnerability.