ArticleInternational journal of molecular sciences2021
The Mechanism of Leptin on Inhibiting Fibrosis and Promoting Browning of White Fat by Reducing ITGA5 in Mice.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- NCOA1 Attenuates High Glucose-Induced Mesangial Matrix Expansion Through ITGA5 Inhibition.Current medical science · 2026Article
- Amniotic extracellular vesicles' effect on equine endometrial cells challenged with LPS: a proteomic analysis.Extracellular vesicles and circulating nucleic acids · 2026Article
- Article
- Claudin Proteins: Their Potential Role in Obesity and Adipose Tissue Signaling, Physiology and Disease.Nutrients · 2025Review
- Impact of leptin on postoperative peritoneal adhesion formations in colorectal resection.International journal of colorectal disease · 2025Article
- Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy.Biomedicines · 2024Article
- A Preliminary Study on Factors That Drive Patient Variability in Human Subcutaneous Adipose Tissues.Cells · 2024Article
- Challenges and opportunities in obesity: the role of adipocytes during tissue fibrosis.Frontiers in endocrinology · 2024Review
- The Combined Partial Knockdown ofAntioxidants (Basel, Switzerland) · 2022Article
- Min pig skeletal muscle response to cold stress.PloS one · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Leptin is a small molecule protein secreted by adipocytes, which can promote white fat browning through activating the hypothalamic nervous system and inhibiting downstream signaling pathways. Moreover, white fat browning has been proven to alleviate fat tissue fibrosis. This study explores the mechanism of leptin in regulating adipose tissue fibrosis and white fat browning. After treating mice with leptin, we screened out the recombinant integrin alpha 5 (ITGA5) through proteomics sequencing, which may play a role in adipose tissue fibrosis. Through real-time quantitative PCR (qPCR), western blotting (WB), hematoxylin-eosin (HE) staining, Masson's trichrome, immunofluorescence, immunohistochemistry, etc., the results showed that after leptin treated adipocytes, the expression of fibrosis-related genes and ITGA5 was significantly down-regulated in adipocytes. We constructed fibrosis model through transforming growth factor-β (TGF-β) and a high-fat diet (HFD), and treated with ITGA5 overexpression vector and interference fragments. The results indicated the expression of fibrosis-related genes were significantly down-regulated after interfering with ITGA5. After treating adipocytes with wortmannin, fibrosis-related gene expression was inhibited after overexpression of ITGA5. Moreover, after injecting mice with leptin, we also found that leptin significantly up-regulated the expression of adipose tissue browning-related genes. Overall, our research shows that leptin can inhibit the activation of phosphatidylinositol 3 kinase (PI3K)-protein kinase B (AKT) signaling pathway by reducing the expression of ITGA5, which could alleviate adipose tissue fibrosis, and further promote white fat browning. Our research provides a theoretical basis for further research on the effect of leptin in fibrosis-related adipose tissue metabolism.
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