ArticleOxidative medicine and cellular longevity2020
SOCS2 Inhibits Mitochondrial Fatty Acid Oxidation via Suppressing LepR/JAK2/AMPK Signaling Pathway in Mouse Adipocytes.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Secretion Patterns of Leptin: A Key Component in the Regulation of Energy Homeostasis and Its Therapeutic Applications.Biomolecules · 2026Review
- Total flavonoids extracted fromTranslational cancer research · 2026Article
- Breaking the metabolic-inflammatory vicious cycle in polycystic ovary syndrome: a comparative review of ketogenic and high-fat diets.Lipids in health and disease · 2025Review
- Uncovering biomarkers and molecular pathways linking NAFLD and AIS: Insights from bioinformatic analysis and experiment.PloS one · 2025Article
- Circular RNA CHACR is involved in the pathogenesis of cardiac hypertrophy.Theranostics · 2025Article
- Analysis of epigenetic clocks links yoga, sleep, education, reduced meat intake, coffee, and a SOCS2 gene variant to slower epigenetic aging.GeroScience · 2024Article
- Oncogenic role of microRNA-19b-3p-mediated SOCS3 in glioma through activation of JAK-STAT pathway.Metabolic brain disease · 2023Article
- JAK2/STAT3 inhibition attenuates intestinal ischemia-reperfusion injury via promoting autophagy: in vitro and in vivo study.Molecular biology reports · 2022Article
- Current knowledge of leptin in wound healing: A collaborative review.Frontiers in pharmacology · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Suppressor of cytokine signaling 2 (SOCS2) plays an important role in fat deposition, skeletal muscle, central nervous system development, and mitochondria biogenesis. Nevertheless, the regulatory mechanisms of SOCS2 on mitochondrial fatty acid oxidation (FAO) remain unclear. Leptin could inhibit food intake and increase thermogenesis through leptin receptor (LepR), which was present in the hypothalamus and certain peripheral organs, including adipose tissue. With strong interest, we focused on the connection between leptin and SOCS2 and their effect on FAO in adipocytes. In our study, we found that the mRNA level of SOCS2 and the protein levels of PGC-1
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