Mechanisms of muscle atrophy: from UPS implication in rodent models to human biomarkers
2022
Taillandier, Daniel | Peris-Moreno, Dulce | Polge, Cécile | Unité de Nutrition Humaine (UNH) ; Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Clermont Auvergne (UCA) | University of Padova
International audience
Показать больше [+] Меньше [-]Английский. The ubiquitin proteasome system (UPS) is a major player of skeletal muscle wasting, a common characteristic of many diseases (cancer, sepsis, heart failure, kidney diseases, etc.) that negatively impacts treatment and life prognosis. In the early 2000, the notion of "atrogenes" (atrophy-related genes) was proposed for genes that were systematically up regulated during catabolic situations in rodents, which included 2 founding members, the E3 ubiquitin ligases MAFbx/Atrogin-1 and MuRF1/TRIM63 [1]. Interestingly, MuRF1 is so far the only E3 ligase known for targeting several sarcomeric proteins (a-actin, MYHC, Troponin I, telethonin) and we recently identified the E2 ubiquitin conjugating enzymes that bring the catalytic activity for MuRF1-dependent protein degradation [2, 3]. Besides rodent models, we and others demonstrated that MAFbx and MuRF1 are also gold standard atrogenes in human pathologies and we recently found that numerous proteins may be part of a muscle atrophy program in chronic kidney disease and lung cancer patients [4]. In addition, we have identified blood markers that reflect skeletal muscle loss in patients suffering from several pathologies.
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