ArticleNature communications2025
Melanocortin 3 receptor regulates hepatic autophagy and systemic adiposity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Melanocortin Receptor Signaling Modulates Anti-Obesity and Glucose Tolerance Effects ofInternational journal of molecular sciences · 2026Article
- Sex-differential associations of MC3R p.F45S with human metabolic profile.Journal of neuroendocrinology · 2026Article
- Effect of a partial loss of function MC3R mutation on MC3R+GHSR-1A heterodimer activity and RNF11 regulation.Journal of endocrinological investigation · 2026Article
- The Genetic Blueprint of Obesity: From Pathogenesis to Novel Therapies.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Review
- Illuminating the Druggable Human Proteome with an AI Protein Profiling Platform.Research square · 2025Article
- Illuminating the Druggable Human Proteome with an AI Protein Profiling Platform.bioRxiv : the preprint server for biology · 2025Article
- Neutrophils at the Crossroads of Inflammatory Bowel Disease and Atherosclerosis: A State-of-the-Art Review.Cells · 2025Review
- Melanocortin 3 receptor regulates hepatic autophagy and systemic adiposity.Nature communications · 2025Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Systemic lipid homeostasis requires hepatic autophagy, a major cellular program for intracellular fat recycling. Here, we find melanocortin 3 receptor (MC3R) regulates hepatic autophagy in addition to its previously established CNS role in systemic energy partitioning and puberty. Mice with Mc3r deficiency develop obesity with hepatic triglyceride accumulation and disrupted hepatocellular autophagosome turnover. Mice with partially inactive human MC3R due to obesogenic variants demonstrate similar hepatic autophagic dysfunction. In vitro and in vivo activation of hepatic MC3R upregulates autophagy through LC3II activation, TFEB cytoplasmic-to-nuclear translocation, and subsequent downstream gene activation. MC3R-deficient hepatocytes had blunted autophagosome-lysosome docking and lipid droplet clearance. Finally, the liver-specific rescue of Mc3r was sufficient to restore hepatocellular autophagy, improve hepatocyte mitochondrial function and systemic energy expenditures, reduce adipose tissue lipid accumulation, and partially restore body weight in both male and female mice. We thus report a role for MC3R in regulating hepatic autophagy and systemic adiposity.
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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.