ArticleCentral-European journal of immunology2021
Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy.
Article in Central-European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Urinary biomarkers associated with podocyte injury in lupus nephritis.Frontiers in pharmacology · 2024Review
- An artificial neural network model based on autophagy-related genes in childhood systemic lupus erythematosus.Hereditas · 2022Article
- Implications of Sphingolipid Metabolites in Kidney Diseases.International journal of molecular sciences · 2022Review
- Vasoactive Drug Therapy and Clinical Nursing of Patients with Cardiovascular Disease.Contrast media & molecular imaging · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLupus nephritis (LN) is a complication of systemic lupus erythematosus (SLE) which seriously threatens the health of people. Tim-1 is known to be associated with the pathogenesis of SLE. However, the role of Tim-1 in LN is still unclear. AIM OF THE STUDY: To explore the expression and the potential regulatory molecular mechanism of Tim-1 in LN-induced podocyte injury. MATERIAL AND
methodsAn in vivo model of LN was established to detect the expression of Tim-1, inflammatory cytokines and autophagy-related proteins. Podocytes were treated with immunoglobulin G (IgG) to establish the LN in vitro model and then treated with an autophagy inhibitor. RT-qPCR and western blot were performed to investigate the effect of Tim-1 on inflammatory responses as well as autophagy in podocytes. The function of Tim-1 in IgG-induced podocytes was detected by CCK-8 and flow cytometry, respectively.
resultsTim-1, L3BII/L3BI ratio and inflammatory cytokines were upregulated in LN mice. Tim-1 notably inhibited IgG-induced inflammatory responses in podocytes via reducing tumor necrosis factor α (TNF-α), interleukin (IL)-6 and IL-1β expression, and it could protect podocytes against LN-induced injury via inducing autophagy. Meanwhile, Tim-1 significantly promoted the proliferation of IgG-induced podocytes via inhibiting apoptosis. The autophagy inhibitor reversed the effect of Tim-1 on inflammatory cytokines and autophagy-related proteins in IgG-treated podocytes.
conclusionsTim-1 protects podocytes against LN-induced injury via mediating autophagy, which might serve as a new target for the treatment of LN.
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