Vitamin D Receptor Deficiency Accelerates Organ-Specific Trajectories of Premature Aging in Mice: The Kidney as the Earliest Target

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Vitamin D Receptor Deficiency Accelerates Organ-Specific Trajectories of Premature Aging in Mice: The Kidney as the Earliest Target

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Co-author 1

Xujiao Chen anjiechen@yeah.net Huashan Hospital Nephrology Shanghai China *

Co-author 2

Huaizhou You huaizhouyou@fudan.edu.cn Huashan Hospital Nephrology Shanghai China -

Co-author 3

Jing Chen 914207568@qq.com Huashan Hospital Nephrology Shanghai China -

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Introduction

Aging is a complex process and demonstrates organ-specific characteristics, but the molecular mechanisms are still not well understood. Vitamin D acts through the vitamin D receptor (VDR), which exhibits strong spatiotemporal specificity. Deficiency in vitamin D/VDR is a global health issue linked to numerous age-related diseases. However, how VDR regulates organ-specific aging remains unclear.

Methods

VDR knockout (KO) mice were generated to observe age-related changes across organs. Single-cell RNA sequencing reveled kidney-specific alterations in cell subtypes. Pericytes and microvascular changes were further assessed by angiography, immunofluorescence, and histopathology. AAV-mediated pericyte-specific VDR knockdown and overexpression models were used to investigate the effects of VDR on microvasculature and renal aging. The impact of VDR on pericyte angiogenic function was further studied using in vitro primary pericyte culture and 3D co-culture systems.

Results

We demonstrated that VDR KO leads to premature aging in organ-specific patterns, with the kidneys emerging as the earliest and most severely affected organ. Single-cell RNA sequencing revealed that pericytes were the most affected kidney cell type, showing pronounced loss, and transdifferentiation into myofibroblasts. The kidney pericyte-specific VDR knockdown mouse model exhibited significant pericyte loss, and microvascular rarefaction, leading to renal aging phenotypes, whereas VDR overexpression alleviated these alterations. In vitro, VDR knockdown enhanced, while VDR activation suppressed pericyte-myofibroblast transdifferentiation, and impaired angiogenic function.

Conclusion

Our findings identify VDR as a crucial factor in governing the organ-specific aging, highlighting the kidney’s early vulnerability to VDR loss, and suggest that targeting pericytes VDR signaling may protect vitamin D deficiency-related aging.

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