Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease with an estimated global prevalence of 24% and to which no effective pharmacological approach has yet been approved. Marta B. Afonso, a Postdoctoral Researcher from iMed.ULisboa, and co-workers have shown that hepatic receptor-interacting protein kinase 3 (RIPK3) correlates with NAFLD severity in humans and mice, playing a key role in managing liver metabolism, damage, inflammation, fibrosis and carcinogenesis. In particular, they found that RIPK3 acts as a lipid metabolism regulator and differentially controls steatosis versus inflammation, likely through peroxisome proliferator-activated receptor γ (PPARγ) modulation. Targeting RIPK3 and its intricate signalling arises as a novel promising approach to treat NAFLD and arrest disease progression.
This study just published in Gut, one of the highest–ranking Gastroenterology journals, was coordinated by Cecília Rodrigues, leader of the Cellular Function and Therapeutic Targeting group, and gathered a unique multidisciplinary international team.
The manuscript can be read here.
Afonso MB, Rodrigues PM, Mateus-Pinheiro M, Simão AL, Gaspar MM, Madji A, Arretxe E, Alonso C, Santos-Laso A, Jiminez-Agüero R, Eizaguirre E, Bujanda L, Pareja MJ, Banales JM, Ratziu V, Gautheron J, Castro RE, Rodrigues CMP. RIPK3 acts as a lipid metabolism regulator contributing to inflammation and carcinogenesis in non-alcoholic fatty liver disease. Gut 2020; 70 (12): 2359-2372. DOI: 10.1136/gutjnl-2020-321767