Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD⁺)-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.

Background: Elevated estrogen has been found to contribute to the pathological development of endometrial cancer (EC), potentially through alterations in the tumor inflammatory immune microenvironment. However, the exact mechanisms underlying this process remain unclear. Methods: Bioinformatics was used to identify differentially expressed genes, analyze pathway enrichment, and assess their correlation with immune cell infiltration. Ishikawa cells and ECC-1 cells were stimulated with estradiol (E2) or the selective estrogen receptor modulator Arzoxifene, and qPCR was performed to measure gene expression changes. CCK8 and FACS assays were used to analyze cell cycle alterations, while Western blotting (WB) was used to evaluate apoptosis. Results: ZNF626 and SLK were highly expressed in EC tissues, whereas RFWD3 expression was downregulated. Immune cell infiltration analysis revealed a positive correlation between ZNF626 and M2 macrophages, while SLK was negatively correlated with M1 macrophages, memory B cells, and plasma cells. RFWD3 showed more complex correlations with multiple immune cell phenotypes, including T cells. E2 stimulation resulted in the increased expression of ZNF626 and SLK, while RFWD3 expression decreased. This was accompanied by enhanced cell proliferation and suppressed apoptosis. In contrast, Arzoxifene stimulation produced the opposite effects. Conclusions: Estrogen promotes cell proliferation and inhibits apoptosis by upregulating ZNF626 and SLK, while downregulating RFWD3. Furthermore, estrogen induces a shift in the tumor microenvironment, characterized by a reduction in memory CD4+ T cells and a transition from M1 to M2 macrophage phenotypes, thus facilitating the onset and progression of EC.