ReviewAdvances in experimental medicine and biology2024
Ubiquitination and Metabolic Disease.
Review in Advances in experimental medicine and biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
The increasing incidence of metabolic diseases, including obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD), in the past decade is a serious concern worldwide. Disruption of cellular protein homeostasis has been considered as a crucial contributor to the pathogenesis of metabolic diseases. To maintain protein homeostasis, cells have evolved multiple dynamic and self-regulating quality control processes to adapt new environmental conditions and prevent prolonged damage. Among them, the ubiquitin proteasome system (UPS), the primary proteolytic pathway for degradation of aberrant proteins via ubiquitination, has an essential role in maintaining cellular homeostasis in response to intracellular stress. Correspondingly, accumulating evidences have shown that dysregulation of ubiquitination can aggravate various metabolic derangements in many tissues, including the liver, skeletal muscle, pancreas, and adipose tissue, and is involved in the initiation and progression of diverse metabolic diseases. In this part, we will summarize the role of ubiquitination in the pathogenesis of metabolic diseases, including obesity, T2DM and NAFLD, and discuss its potential as a therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.