Effects of Aging on Diabetic Kidney Disease and Extracellular Vesicles Based Therapeutic Responses

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Effects of Aging on Diabetic Kidney Disease and Extracellular Vesicles Based Therapeutic Responses

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Co-author 1

Jiaxuan Wang wang.jiaxuan@Mayo.edu Mayo Clinic Division of Nephrology and Hypertension Jacksonville United States *

Co-author 2

Caroline J. Zinn zinn.caroline@mayo.edu Mayo Clinic Division of Nephrology and Hypertension Jacksonville United States -

Co-author 3

Maya Learmonth learmonth.maya@mayo.edu Mayo Clinic Division of Nephrology and Hypertension Jacksonville United States -

Co-author 4

Atta Behfar Behfar.Atta@mayo.edu Mayo Clinic Cardiovascular Medicine Rochester United States -

Co-author 5

Joy Wolfram j.wolfram@uq.edu.au University of Queensland School of Chemical Engineering Brisbane Australia -

Co-author 6

LaTonya J. Hickson Hickson.LaTonya@mayo.edu Mayo Clinic Nephrology and Hypertension Jacksonville United States -

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Introduction

Diabetes mellitus is the leading cause of kidney failure in the United States. Age-related pathological conditions, including diabetes and diabetic kidney disease (DKD), accelerate renal aging and heighten vulnerability to irreversible kidney injury. Individuals aged 75 years and older account for approximately 40% of end-stage kidney disease cases. Cellular senescence drives DKD progression by promoting chronic inflammation, fibrosis, and tissue dysfunction. Extracellular vesicles (EVs) have emerged as a promising cell-based therapeutic strategy due to their anti-inflammatory and anti-fibrotic properties. This study aims to compare DKD-associated senescence and therapeutic responses between young and aged DKD models following platelet-derived extracellular vesicle (PEV) treatment.

Methods

A streptozotocin-induced Type 1 diabetes model was established in young (8-week-old) and aged (17-month-old) C57BL/6J mice. Mice with fasting blood glucose > 250 mg/dL were considered diabetic and, after 11 weeks, received either saline or PEV (4 × 10¹⁰ EVs/mice; 125 µL/day for two days). Kidneys were collected at one and two weeks post-treatment for histological and molecular assessment of senescence (SA-β-gal staining, p16^INK4a, p21^CDKN1A, and p19 expression) and inflammatory markers.

Results

Transcriptomic profiling revealed that aging significantly amplified DKD-associated senescence and inflammatory signatures, with ~350 differentially expressed genes in aged versus young DKD mice compared to ~50 in healthy control age comparison. SenMayo gene sets were enriched in aged DKD kidneys, alongside elevated p21, p16, and p19 expression. PEV treatment reduced p21 at one week and p16 at two weeks in young DKD mice, suggesting potential attenuation of senescence responses.

Conclusion

Aging exacerbates DKD-associated senescence and injury, while PEVs demonstrate potential as senotherapeutic and regenerative agents. Ongoing work will evaluate PEV efficacy in aged DKD and optimize treatment strategies for older individuals.

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