Tier 3 — preclinical

Urolithin A protects against calcium oxalate-induced crystal formation and kidney injury by regulating PCK1 to restore mitophagy function in kidney stone disease

Sun X, Gao C, Zhang P, Peng Y, Wang M, Liu J, Ma C, Li S, Xia Z
Biochimica et Biophysica Acta - Molecular Basis of Disease 2026 1872(3):168106

Bibliography

PubMed
PMID 41265017
DOI
10.1016/j.bbadis.2025.168106

Study snapshot

DesignIn vivo mouse calcium-oxalate injury model plus in vitro renal tubular-cell mechanistic experiments
ModelMouse kidney stone/oxalate injury model and renal tubular epithelial cells
SampleMultiple preclinical cohorts
InterventionUrolithin A with PCK1 pathway manipulation
DurationExperimental model dependent
EndpointsCalcium oxalate crystal deposition; Renal function and injury; Mitophagy; Oxidative stress and apoptosis; PCK1 expression

What the study showed, in plain terms

Urolithin A reduced calcium-oxalate crystal deposition and kidney injury in mice while restoring mitophagy through a PCK1-linked pathway. This is useful renal mechanism evidence but does not show that Urolithin A prevents kidney stones in people.

Key findings

Renal calcium-oxalate deposition and injury were reduced in mice.

Mitophagy and mitochondrial homeostasis improved.

PCK1 was identified as an important downstream mediator.

What this study can and cannot tell us

No human supplementation trial was performed.

Kidney-stone prevention and recurrence outcomes in people are unknown.

The disease model is mechanistic and preclinical.

Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology