ArticleOncotarget2017
αMSH inhibits adipose inflammation via reducing FoxOs transcription and blocking Akt/JNK pathway in mice.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Notch2 Directs aTreg Cell Fate Toward Immunoregulation or Inflammatory Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor.EMBO reports · 2024Article
- Melanocortin-5 Receptor: Pharmacology and Its Regulation of Energy Metabolism.International journal of molecular sciences · 2022Review
- Characterization of the chicken melanocortin 5 receptor and its potential role in regulating hepatic glucolipid metabolism.Frontiers in physiology · 2022Article
- Antifibrotic and Anti-Inflammatory Actions of α-Melanocytic Hormone: New Roles for an Old Player.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Altered features of neurotransmitters: NPY, α-MSH, and AgRP in type 2 diabetic patients with hypertension.The Journal of international medical research · 2020Observational
- circARF3 Alleviates Mitophagy-Mediated Inflammation by Targeting miR-103/TRAF3 in Mouse Adipose Tissue.Molecular therapy. Nucleic acids · 2019Article
- ARPE-19-derived VEGF-containing exosomes promote neovascularization in HUVEC: the role of the melanocortin receptor 5.Cell cycle (Georgetown, Tex.) · 2019Article
- miR-103/107 promote ER stress-mediated apoptosis via targeting the Wnt3a/β-catenin/ATF6 pathway in preadipocytes.Journal of lipid research · 2018Article
- An Integrated Proteomics and Bioinformatics Approach Reveals the Anti-inflammatory Mechanism of Carnosic Acid.Frontiers in pharmacology · 2018Article
- Homeobox a5 Promotes White Adipose Tissue Browning Through Inhibition of the Tenascin C/Toll-Like Receptor 4/Nuclear Factor Kappa B Inflammatory Signaling in Mice.Frontiers in immunology · 2018Article
- Hoxa5 increases mitochondrial apoptosis by inhibiting Akt/mTORC1/S6K1 pathway in mice white adipocytes.Oncotarget · 2017Article
- ColXV promotes adipocyte differentiation via inhibiting DNA methylation and cAMP/PKA pathway in mice.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpha melanocyte stimulating hormone (αMSH) abates inflammation in multiple tissues, while Forkhead box proteins O (FoxOs) stimulate inflammatory cascade. However, the relationship between αMSH and FoxOs in adipose inflammation remains unclear. In this study, we used LPS-induced inflammation model, attempted to interpret the function of αMSH in inflammation and the interactions with FoxOs. Results indicated that upon inflammatory situation, the secretion of αMSH and the expression of its receptor MC5R were greatly decreased, but FoxOs expressions were elevated. After the treatment with αMSH, LPS-induced adipose inflammation together with FoxOs expressions was significantly reduced. Conversely, when Foxo1, Foxo3a or Foxo4 overexpressed in αMSH treated inflammatory mouse model, all the anti-inflammatory impacts of αMSH were found disappeared. We further studied the mechanisms by which αMSH exerts its anti-inflammatory impacts and how FoxOs reverse αMSH's function. Foxo4 was found as a negative regulator for MC5R transcription in αMSH inhibited inflammation. Moreover, a negative role was found of αMSH in regulating both Akt and JNK signal pathways by observing the enhanced the anti-inflammatory impacts of pathway-specific inhibitors with αMSH treatment. Our findings demonstrate αMSH plays a key role in the prevention of adipose inflammation and inflammatory diseases by down-regulating Akt/JNK signal pathway and negatively interacting with FoxOs, which brings up αMSH as a novel candidate factor in the adipose anti-inflammation process in obesity.
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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 Socratic graph.