Vdr, the Vitamin D receptor, is a nuclear receptor that mediates the biological functions of 1α,25-dihydroxyvitamin D3. It plays essential roles in regulating cell proliferation, barrier function, and immunity, especially in the intestine [4]. Vdr is also involved in multiple signaling pathways, such as those related to inflammation, immune responses, and carcinoma inhibition [3]. Genetic models, like gene knockout mouse models, are valuable for studying Vdr's functions.

In a VDR gene knockout mouse model of cardiac steatosis, VDR deficiency enhanced the pathological phenotype, including increased myocyte size, cardiac hypertrophy markers, interstitial fibrosis, and reduced cardiac function, suggesting VDR's role in modulating disease severity in cardiovascular disorders [5]. In PD, the VDR FokI (rs2228570) polymorphism was associated with the disease, with the TT genotype and T allele being risk factors, especially in male patients, and a "risk" haplotype was identified [6]. In diabetic rats, VDR agonists ameliorated renal tubulointerstitial fibrosis by regulating mitochondrial function, and VDR restored mitophagy through the Mfn2-MAMs-Fundc1 pathway [1]. High VDR expression in pancreatic cancer promoted M2 macrophage polarization and recruitment via CCL20 secretion, activating tumor progression [2].

In conclusion, Vdr is crucial in various biological processes and diseases. Gene knockout models have revealed its roles in cardiovascular diseases, Parkinson's disease, diabetic renal injury, and pancreatic cancer. Understanding Vdr's functions can provide insights into disease mechanisms and potential therapeutic strategies for these conditions.