Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Objective: To investigate the expression of Stim1 in the kidneys of mice with lupus, and the effect of Stim1 on the progression of renal interstitial fibrosis.
Methods: Mice (MRL/lpr) with spontaneous lupus nephritis (LN) and normal control mice (C57/BL) were selected. Immunohistochemistry and Masson staining were used to determine the degree of renal interstitial fibrosis in kidney tissues. The expression of Stim1 and fibronectin in tissues was measured by qRT-PCR, western blotting, and immunohistochemistry. Urine protein, blood urea nitrogen, and serum creatinine levels in the mice were analyzed, and Spearman analysis was conducted to determine the correlation with Stim1 expression levels. Mouse renal tubular epithelial cells (mRTECs) were chosen as the experimental objects. After various treatments, the cells were divided into the blank control group, lipopolysaccharide (LPS) treatment group, LPS+siRNA-NC group and LPS+siRNA-Stim1 group. Western blotting and immunofluorescence were used to measure epithelial-mesenchymal transition (EMT)-related protein levels.
Results: There was significant interstitial fibrosis in the kidneys of LN mice. Compared with that in normal mice, the expression of Stim1 in the kidney tissues of LN mice was significantly increased, and Stim1 expression was positively correlated with fibronectin, urine protein, blood urea nitrogen and serum creatinine levels. LPS induced the expression of Stim1, fibronectin, and α-SMA in mRTECs and decreased the protein level of E-CA, while silencing Stim1 effectively alleviated the effects of LPS.
Conclusion: Stim1 is significantly increased in the kidneys of lupus mice, and it is possible to promote EMT in renal tubular epithelial cells and renal interstitial fibrosis by elevating fibronectin, which ultimately contributes to renal damage.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791395 | PMC |
Publication Analysis
Top Keywords
Similar Publications
Bifunctional adECM bioscaffold with STIM1-ASCs and IGF-2 promotes functional masseter VML repair via myogenesis and fibrosis suppression.
Bioact Mater
December 2025
Department of Plastic Surgery, Peking University Third Hospital, Beijing, 100191, China.
Craniofacial muscles are essential for a variety of functions, including fine facial expressions. Severe injuries to these muscles often lead to more devastating consequences than limb muscle injuries, resulting in the loss of critical functions such as mastication and eyelid closure, as well as facial aesthetic impairment. Therefore, the development of targeted repair strategies for craniofacial muscle injuries is crucial.
View Article and Find Full Text PDFTRPV6-mediated store-operated Ca entry participates in pancreatic acinar cell injury during acute pancreatitis.
Cell Mol Gastroenterol Hepatol
September 2025
West China Centre of Excellence for Pancreatitis, Institute of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu, China. Electronic address:
Background & Aims: Suppressing toxic Ca accumulation in pancreatic acinar cells (PACs) is the central therapeutic strategy of acute pancreatitis (AP). Store-operated Ca entry (SOCE) represents an important mechanism promoting Ca overload, which remains incompletely understood in AP. Transient receptor potential vanilloid 6 (TRPV6) is an ion channel highly selective to Ca, and its role in PACs or AP onset remains largely unknown.
View Article and Find Full Text PDFDefining the interactome of the pancreas-specific SPCA2 isoform (SPCA2C) identifies unique links to store-operated Ca entry.
FEBS J
August 2025
Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Canada.
Calcium (Ca) is critical for normal cell function, and several protein networks are required for Ca signaling. In the pancreas, regulated changes in cytosolic Ca allow for the exocytosis of zymogen granules, and altered Ca signaling underlies pancreatic pathologies. Previously, our laboratory showed a pancreas-specific isoform of secretory pathway Ca-ATPase 2 (also known as calcium-transporting ATPase type 2C member 2; SPCA2), termed SPCA2C (gene name Atp2c2c, C-terminally truncated form), affects multiple pathways involved in Ca homeostasis.
View Article and Find Full Text PDFTranscription factor MAFA regulates muscle growth via calcium ion channels and receptor tyrosine kinase activation.
Int J Biol Macromol
September 2025
College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China; Key Laboratory of Animal Production and Product Quality and Safety, Ministry of Education, Changchun 130118, China. Electronic address:
MAFA, a member of the large Maf transcription factor family, is known primarily for its role in regulating insulin gene expression. However, its function in non-pancreatic tissues remains largely unexplored. This study aims to investigate the role of MAFA in skeletal muscle and to elucidate the underlying molecular mechanisms.
View Article and Find Full Text PDFEarly cardioprotective effects of SGLT2i on hypertensive cardiac remodeling via STIM1/Orai1-dependent calcium signaling: beyond blood pressure control.
J Bioenerg Biomembr
July 2025
Department of Cardiology, National Cardiovascular Disease Regional Center for Anhui, the First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui, China.
The cardioprotective effects of sodium-glucose cotransporter-2 inhibitors (SGLT2i) have attracted significant attention. The calcium ion signaling pathway influences various aspects of cellular function, store-operated calcium channels (SOCCs) serve as key calcium ion channels that induce cell apoptosis and exacerbate cardiac remodeling. This study aims to investigate the effects of SGLT2i on SOCCs and its potential cardioprotective mechanisms.
View Article and Find Full Text PDF