ArticleImmunity, inflammation and disease2023
Knockdown of KLF5 ameliorates renal fibrosis in MRL/lpr mice via inhibition of MX1 transcription.
Article in Immunity, inflammation and disease, 2023. 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, 7 citations in OpenAlex.
- KLF transcription factors in metabolic kidney disease: from podocyte protection to tubulointerstitial fibrosis.International urology and nephrology · 2026Review
- YAP/TAZ inhibition refines TGF-β signaling to prevent laryngeal fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Discovery of core genes for systemic lupus erythematosus via genome-wide aggregated trans-effects analysis.Genes and immunity · 2025Article
- Identification and immunoassay of biomarkers associated with T cell exhaustion in systemic lupus erythematosus.Frontiers in immunology · 2025Article
- HDAC6 promotes inflammation in lupus nephritis mice by regulating transcription factors MAFF and KLF5 in renal fibrosis.Renal failure · 2024Article
- Multi-omics differences in the bone marrow between essential thrombocythemia and prefibrotic primary myelofibrosis.Clinical and experimental medicine · 2024Article
- Transcription Factors in the Pathogenesis of Lupus Nephritis and Their Targeted Therapy.International journal of molecular sciences · 2024Review
- Exploring the shared gene signatures and mechanism among three autoimmune diseases by bulk RNA sequencing integrated with single-cell RNA sequencing analysis.Frontiers in molecular biosciences · 2024Article
- Knockdown of KLF5 ameliorates renal fibrosis in MRL/lpr mice via inhibition of MX1 transcription.Immunity, inflammation and disease · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aims to elucidate the role of Kruppel-like factor (KLF5) and myxovirus resistance 1 (MX1) in the progression of renal fibrosis in lupus nephritis (LN).
methodsFirst, the expression of KLF5 and MX1 was assessed in the peripheral blood of LN patients and healthy participants. Next, the pathological changes in renal tissues were evaluated and compared in BALB/c and MRL/lpr mice, by detecting the expression of fibrosis marker proteins (transforming growth factor-β [TGF-β] and CTGF) and α-SMA, the content of urine protein, and the levels of serum creatinine, blood urea nitrogen, and serum double-stranded DNA antibody. In TGF-β1-induced HK-2 cells, the messenger RNA levels of KLF5 and MX1 were tested by qRT-PCR, and the protein expression of α-SMA, type I collagen (Col I), fibronectin (FN), and matrix metalloproteinase 9 (MMP9) was measured by western blot analysis. Moreover, the relationship between KLF5 and MX1 was predicted and verified.
resultsIn renal tissues of MRL/lpr mice and the peripheral blood of LN patients, KLF5 and MX1 were highly expressed. Pearson analysis revealed that KLF5 was positively correlated with MX1. Furthermore, KLF5 bound to MX1 promoter and promoted its transcription level. MRL/lpr mice showed substantial renal injury, accompanied by increased expression of α-SMA, TGF-β, CTGF, Col I, FN, and MMP9. Injection of sh-KLF5 or sh-MX1 alone in MRL/lpr mice reduced renal fibrosis in LN, while simultaneous injection of sh-KLF5 and ad-MX1 exacerbated renal injury and fibrosis. Furthermore, we obtained the same results in TGF-β1-induced HK-2 cells.
conclusionKnockdown of KLF5 alleviated renal fibrosis in LN through repressing the transcription of MX1.
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