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Diabetic kidney disease (DKD) is one of the common and serious complications of diabetes mellitus, with a complex pathogenesis and a lack of ideal treatment options in clinical practice. In recent years, the protective role of vitamin D and its receptor signaling pathway in DKD has garnered widespread attention. Vitamin D plays an important role in the onset and progression of DKD by participating in the regulation of insulin secretion, inhibiting inflammatory responses, attenuating podocyte injury, modulating the renin-angiotensin system (RAS), and inhibiting renal interstitial fibrosis through its receptor (VDR). Studies on the use of vitamin D and its receptors in DKD have increased gradually in recent years, with a focus on the development of vitamin D analogs and the clinical application of VDR activators. This study reviewed the mechanisms of vitamin D and its receptor in diabetic nephropathy, as well as the potential for therapeutic applications and associated adverse effects. It also analyzed current research hotspots and development trends based on bibliometrics. Future research should focus on further optimizing vitamin D-based therapeutic strategies to achieve better clinical efficacy and safety.
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Adv Sci (Weinh)
September 2025
State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, P. R. China.
Perineural invasion (PNI) is a common pathological characteristic of pancreatic ductal adenocarcinoma (PDAC), closely linked to postoperative recurrence, metastasis, and unfavorable prognosis. Nevertheless, the precise mechanisms that govern PNI in PDAC remain poorly elucidated. Here, group-specific component protein (GC) is identified as one of the most significantly upregulated genes related to PNI, primarily derived from malignant ductal cells compared to other cell types.
View Article and Find Full Text PDFOsteoporos Int
September 2025
Department of Rheumatology, Univ. Lille, CHU Lille, MABlab ULR 4490, 59000, Lille, France.
Medications like liraglutide 3.0 mg daily (Saxenda®; Novo Nordisk) and semaglutide 2.4 mg weekly (Wegovy®; Novo Nordisk), which are glucagon-like peptide-1 receptor agonists (GLP-1Ra), have been sanctioned for prolonged weight management in people living with obesity (PwO).
View Article and Find Full Text PDFInt J Cancer
September 2025
Department of Biomedical Engineering, Virginia Commonwealth University, Richmond, Virginia, USA.
This study examined the effects of 24R,25-dihydroxyvitamin D (24R,25(OH)D) in estrogen-responsive laryngeal cancer tumorigenesis in vivo, the mechanisms involved, and whether the ability of the tumor cells to produce 24R,25(OH)D locally is estrogen-dependent. Estrogen receptor alpha-66 positive (ER+) UM-SCC-12 cells and ER- UM-SCC-11A cells responded differently to 24R,25(OH)D in vivo; 24R,25(OH)D enhanced tumorigenesis in ER+ tumors but inhibited tumorigenesis in ER- tumors. Treatment with 17β-estradiol (E) for 24 h reduced levels of CYP24A1 protein but increased 24R,25(OH)D production in ER+ cells; treatment with E for 9 min reduced CYP24A1 at 24 h and reduced 24R,25(OH)D production in ER- cells.
View Article and Find Full Text PDFJ Pharm Pract
September 2025
ICPS, Pharmacovigilance & Clinical Research, Department of Biomedical and Clinical Sciences, University Hospital Luigi Sacco, Università Degli Studi di Milano, Milan, Italy.
Olmesartan, an angiotensin II receptor blocker (ARB) approved in 2002, is used to treat hypertension, either alone or with other antihypertensive drugs. It has been frequently associated with sprue-like enteropathy, while few cases of colitis have been reported. Differentiating between sprue-like enteropathy and colitis is of clinical concern, since just the first condition is a well-documented adverse event of olmesartan.
View Article and Find Full Text PDFAnn Plast Surg
September 2025
From the Department of Plastic Surgery, Section of Surgical Sciences, Vanderbilt University Medical Center, Nashville, TN.
Hypertrophic scarring (HTS) remains a critical challenge in burn care, often resulting in debilitating contractures, chronic pain, and significant psychosocial burden. While current treatment emphasizes structural repair, recent advances underscore the importance of addressing the biological drivers of fibrosis. This review synthesizes evolving strategies in burn scar prevention, highlighting tissue-engineered matrices, autologous cell therapies, and predictive molecular tools that shift care from reactive to regenerative.
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