ArticleCell death & disease2022
Latexin deficiency attenuates adipocyte differentiation and protects mice against obesity and metabolic disorders induced by high-fat diet.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Ssu72 phosphatase orchestrates obesogenic adipogenesis and metabolic homeostasis during nutrient excess.Cell death and differentiation · 2026Article
- Functions of dendrobine in a zebrafish model of diabetic retinopathy.Journal of translational medicine · 2026Article
- Article
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
- Latexin deficiency limits foam cell formation and ameliorates atherosclerosis by promoting macrophage phenotype differentiation.Cell death & disease · 2024Article
- Pancreatic cancer stemness: dynamic status in malignant progression.Journal of experimental & clinical cancer research : CR · 2023Review
- Loss of LXN promotes macrophage M2 polarization and PD-L2 expression contributing cancer immune-escape in mice.Cell death discovery · 2022Article
- Association of Body Composition with Pulmonary Function in Ningxia: The China Northwest Cohort.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Obesity is a risk factor for many chronic diseases, and is associated with increased incidence rate of type 2 diabetes, hypertension, dyslipidemia and cardiovascular diseases. Adipocyte differentiation play critical role during development of obesity. Latexin (LXN), a mammalian carboxypeptidase inhibitor, plays important role in the proliferation and differentiation of stem cells, and highlights as a differentiation-associated gene that was significantly downregulated in prostate stem cells and whose expression increases through differentiation. However, it is unclear whether LXN is involved in adipocyte differentiation. The aim of this study was to evaluate the role of LXN on adipocyte differentiation, as well as its effects on high fat-induced obesity and metabolic disorders. In this study, we determine the expression of LXN in adipose tissue of lean and fat mice by Western blot, qPCR and immunohistochemistry. We found that LXN in fat tissues was continuous increased during the development of diet-induced obesity. We fed wild-type (WT) and LXN
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