Activation of hypothalamic AMPK ameliorates metabolic complications of experimental arthritis.
Patricia Seoane-CollazoEva Rial-PensadoÁnxela Estévez-SalgueroEdward MilbankLucía García-CaballeroMarcos RíosLaura Liñares-PoseMorena ScoteceRosalía GallegoJosé Manuel Fernández-RealRubén NogueirasCarlos DiéguezOreste GualilloMiguel LópezPublished in: Arthritis & rheumatology (Hoboken, N.J.) (2021)
Overall, these data indicate that EA promotes a central catabolic state that can be targeted and reversed by the activation of hypothalamic AMPK. This might open new therapeutic alternatives to treat rheumatoid arthritis (RA)-associated metabolic comorbidities, improving RA-patients overall prognosis.
Keyphrases
- rheumatoid arthritis
- disease activity
- end stage renal disease
- ejection fraction
- ankylosing spondylitis
- newly diagnosed
- chronic kidney disease
- interstitial lung disease
- minimally invasive
- prognostic factors
- risk factors
- cancer therapy
- electronic health record
- systemic lupus erythematosus
- patient reported outcomes
- drug delivery
- idiopathic pulmonary fibrosis
- artificial intelligence