ArticleCell death & disease2023
Elevated fatty acid β-oxidation by leptin contributes to the proinflammatory characteristics of fibroblast-like synoviocytes from RA patients via LKB1-AMPK pathway.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Low-dose oral nicotinamide mononucleotide for immune thrombocytopenia: a phase 1/2 trial.Nature medicine · 2026Trial
- Review
- Leptin Signaling at the Crossroads of Obesity, Immunity, and Cancer: Mechanistic Insights and Therapeutic Implications.Biomolecules & therapeutics · 2026Review
- IMP2 enhances M2 macrophage polarization via LKB1-AMPK-mediated mitochondrial dynamics and fatty acid β-oxidation to ameliorate diabetic osteoporosis.Cellular and molecular life sciences : CMLS · 2026Article
- The incretin-joint axis: weight-independent mechanisms and disease-modifying potential in chronic arthropathies.Rheumatology advances in practice · 2026Review
- Identification and Immune Landscape Analysis of Fatty Acid Metabolism-related Genes Associated with Rheumatoid Arthritis.International journal of medical sciences · 2026Article
- Combination of Chenpi and Banxia alleviates synovial inflammation in a rat model of rheumatoid arthritis by targeting the JNK/AP-1 signaling pathway.Frontiers in immunology · 2026Article
- Fatty Acid Metabolic Reprogramming in Rheumatoid Arthritis: Integrating Inflammation, Resolution Failure, and Joint Destruction.Journal of inflammation research · 2026Review
- A New N6-Methyladenosine Inhibitor, Celastrol, Alleviates Rheumatoid Arthritis via Targeting IGF2BP3.MedComm · 2025Article
- Activation of eIF2α-ATF4 by endoplasmic reticulum-mitochondria coupling stress enhances COX2 expression and MSC-based therapeutic efficacy for rheumatoid arthritis.Stem cell research & therapy · 2025Article
- Inhibition of Aberrant Activated Fibroblast-Like Synoviocytes in Rheumatoid Arthritis by Leishmania Peptide via the Regulation of Fatty Acid Synthesis Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Time-restricted feeding alleviates arthritis symptoms augmented by high-fat diet.Frontiers in immunology · 2025Article
- Crossing the metabolic homeostasis divide: panoramic decoding of therapeutic targets for metabolic-inflammatory crosstalk in rheumatoid arthritis.Frontiers in immunology · 2025Review
- Metabolic reprogramming: the central mechanism driving inflammatory polarization in rheumatoid arthritis and the regulatory role of traditional Chinese medicine.Frontiers in immunology · 2025Review
- TLR2 reprograms glucose metabolism in CD4Clinical rheumatology · 2024Article
- The expression of RBPJ and its potential role in rheumatoid arthritis.BMC genomics · 2024Article
- Review
- Leveraging altered lipid metabolism in treating B cell malignancies.Progress in lipid research · 2024Review
- LKB1 biology: assessing the therapeutic relevancy of LKB1 inhibitors.Cell communication and signaling : CCS · 2024Review
- Metabolic changes in fibroblast-like synoviocytes in rheumatoid arthritis: state of the art review.Frontiers in immunology · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast-like synoviocytes (FLS) maintain chronic inflammation leading to joint destruction in rheumatoid arthritis (RA). Fatty acid β-oxidation (FAO) regulates cell function. Here, we aimed to investigate the effect of FAO enhanced by leptin on the characteristics of RA-FLS and elucidate the potential metabolic mechanism. Key enzymes involved in lipid metabolism were detected with qPCR in HSF, MH7A cell line and isolated RA-FLS treated with RA or healthy control (HC) serum. In some experiments, FAO inhibitor, etomoxir (ETO) or anti-leptin antibody were added into serum-treated RA-FLS. In other experiments, RA-FLS were stimulated with leptin together with ETO or AMP-activated protein kinase (AMPK) inhibitor compound C (CC) or silencing liver kinase B1 (LKB1). Cell proliferation, proinflammatory factor production, pro-angiogenesis, chemoattractive potential, FAO-related key enzymes, AMPK and LKB1 in FLS were analyzed. FAO-related key enzymes were evaluated in serum-treated RA-FLS with or without anti-leptin antibody. Related functions of leptin-stimulated RA-FLS were examined in the presence or absence of ETO. AMP-activated protein kinase (AMPK) and liver kinase B1 (LKB1) in leptin-stimulated RA-FLS were tested with western blot. Activation of AMPK in leptin-stimulated RA-FLS was detected after silencing LKB1. We found that MH7A cell line and RA serum-treated FLS exhibited upregulated FAO, and ETO could inhibit the proinflammatory phenotypes of RA-FLS. The addition of anti-leptin antibody suppressed the elevation of FAO mediated by RA serum. More importantly, leptin promoted the proinflammatory characteristics of RA-FLS, which was reversed by ETO. Leptin activated AMPK by upregulating LKB1. CC impaired leptin-induced CPT-1A expression in RA-FLS. Our study uncovers that elevated FAO mediated by leptin drives abnormal function of RA-FLS and suggests leptin or FAO inhibition may serve as a promising therapeutic strategy for RA.
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