Synapse
⌘+K
Synapse
PulseExploreJournal ClubResearchersJournals
Instagram
HomeJournal ClubExplore
September 5, 2026International Journal of Molecular SciencesOpen Access

Elevated Prorenin Induces Podocyte Injury and Glomerular Fibrosis in cyp1a1-Prorenin Transgenic Rats

View Full Paper
Ask AI
Bookmark
Share

Why the study?

Elevated plasma prorenin is linked to albuminuria and diabetic nephropathy progression, but its pathogenic role in podocyte dysfunction warrants further investigation.

Does elevated prorenin induce podocyte injury and glomerular fibrosis in a transgenic rat model?

Population

cyp1a1-prorenin transgenic rats and wild-type control rats

Comparison

Indole-3-carbinol diets (0.05%, 0.15%, or 0.3%) vs wild-type normal diet, plus amlodipine or enalapril

Design

Randomized animal study

Key result

Inducing elevated prorenin with 0.05%, 0.15%, or 0.3% indole-3-carbinol in transgenic rats dose-dependently increased mean arterial pressure, podocyte injury, and glomerular fibrosis.

Authors

CGChunyan GuXLXia LiuJWJie Wu

Discussion

Loading...

Member takes

Overview

Should not change clinical practice; extends experimental evidence for prorenin in glomerular injury but requires human validation.

Key Points

  • To determine whether elevated plasma prorenin directly promotes podocyte dysfunction, albuminuria, and glomerular fibrosis using an inducible transgenic rat model.
  • Randomized cyp1a1-prorenin transgenic rats to receive diets containing 0.05%, 0.15%, or 0.3% of the gene activator indole-3-carbinol (I3C) for 4 weeks alongside wild-type controls.
  • Administered 6-week treatment regimens of either amlodipine or enalapril to evaluate blood pressure control and suppression of inflammatory and oxidative pathways.
  • Induction of prorenin caused dose-dependent increases in mean arterial pressure and urinary albumin excretion while reducing podocyte counts and slit diaphragm protein expression.
  • Prorenin elevation stimulated profibrotic factors and glomerular fibrosis, which were only partially attenuated by enalapril or amlodipine through NF-κB and Nox2 pathway suppression.

Structured PICO

Does elevated prorenin induce podocyte injury and glomerular fibrosis in a transgenic rat model?

P
Population
cyp1a1-prorenin transgenic rats randomized to receive diets containing increasing concentrations of indole-3-carbinol for 4 weeks.
I
Intervention
Diets containing indole-3-carbinol (I3C; 0.05%, 0.15%, or 0.3%) for 4 weeks to induce prorenin expression, followed by treatment with amlodipine or enalapril for 6 weeks
C
Comparator
Wild-type rats maintained on a normal diet
O
Outcome
Podocyte injury (podocyte number, slit diaphragm protein expression, foot process effacement, podocyte hypertrophy) and glomerular fibrosissurrogate

Elevated prorenin promotes podocyte injury and glomerular fibrosis through both angiotensin II-dependent and independent pathways, highlighting its pathogenic role in nephropathy.

Cite This Study

Gu et al. (2026) studied Podocyte injury and glomerular fibrosis. Indole-3-carbinol (I3C) diet vs. Wild-type rats on a normal diet was evaluated on Podocyte injury and glomerular fibrosis. Inducing elevated prorenin with 0.05%, 0.15%, or 0.3% indole-3-carbinol in transgenic rats dose-dependently increased mean arterial pressure, podocyte injury, and glomerular fibrosis.

synapsesocial.com/papers/6a9bd4346b95aff0620eba85https://doi.org/10.3390/ijms27177888
View Full Paper
Ask AI
Bookmark
Share