AI Article Synopsis
- Diabetic nephropathy (DN) is a complication from diabetes characterized by the proliferation of glomerular mesangial cells (GMCs), which is influenced by increased levels of Stromal interaction molecule 1 (STIM1).
- The study demonstrated that high glucose conditions increased STIM1 levels in both diabetic rat renal tissues and HBZY-1 cells, and that reducing STIM1 activity led to suppressed cell proliferation and fibrosis through the activation of autophagy.
- STIM1 regulates these processes via the PI3K/AKT/mTOR signaling pathway, suggesting it could be a potential target for DN treatment.
Article Abstract
Diabetic nephropathy (DN) is a renal microvascular complication caused by diabetes mellitus. One of the most typical characteristics of DN is glomerular mesangial cells (GMCs) proliferation. Stromal interaction molecule 1 (STIM1), a Ca channel, is involved in many diseases. In this study, we investigated the role of STIM1 in the proliferation and fibrosis in high glucose (HG)-induced HBZY-1 cells. We found that the expression of STIM1 was increased in renal tissues of diabetic rat and HBZY-1 cells stimulated by HG. Downregulation of STIM1-mediated SOCE suppressed hyperglycemic cell proliferation and fibrosis by activating autophagy. In addition, the inhibitory effect of downregulating STIM1 on cells was blocked by autophagy inhibitor Bafilomycin A1 (BafA1). Moreover, this experiment also showed that STIM1 regulated autophagy, cell proliferation and fibrosis via PI3K/AKT/mTOR signal pathway. These results clarify the role of STIM1 in HBZY-1 cells and its mechanism, and provide a new target for the treatment of DN.
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| http://dx.doi.org/10.1007/s11010-023-04844-7 | DOI Listing |
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