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Published on: September 1, 2016
Multiple mechanisms in renal artery stenosis-induced renal interstitial fibrosis
1Department of Nephrology, 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
Background/Aims:
Renal artery stenosis (RAS), which may lead to renal fibrosis, is a common cause of end-stage renal disease in elderly patients. However, the potential mechanisms leading to the development of renal fibrosis and atrophy have not been clarified.
Methods:
A two-kidney, one-clip Goldblatt mouse model was established in the present study. Blood pressure, morphological and pathological alterations were examined on days 7, 14, and 28 after surgery. Peritubular capillary loss and pericyte changes after injury were evaluated. Inflammatory macrophage infiltration and Wnt/β-catenin signaling were also investigated.
Results:
A significant increase in blood pressure and obvious renal atrophy were observed on days 7, 14, and 28 after surgery. Following surgery, the clipped kidneys developed aggravated interstitial fibrosis and tubular epithelial injury over time. Moreover, RAS induced obvious peritubular capillary loss and inflammatory macrophage infiltration. Increased pericyte number was found in the clipped kidneys, but these cells detached from the endothelial cells and migrated to the interstitium. Wnt/β-catenin signaling was also significantly upregulated in the clipped kidneys after surgery.
Conclusion:
Our study provides a novel insight into the mechanisms linking peritubular capillary loss and pericyte changes in RAS-induced renal fibrosis. Our findings also suggest that inflammatory macrophages and Wnt/β-catenin signaling participate in these pathological processes. Therefore, multi-target therapeutic strategies may significantly contribute to the prevention of renal interstitial fibrosis and the preservation of renal function in patients with RAS.
Insights
Renal artery stenosis (RAS) causes kidney damage and fibrosis through peritubular capillary loss and altered pericytes. Inflammatory macrophages and Wnt/β-catenin signaling are key contributors to this process.
Area of Science:
- Nephrology
- Pathology
- Molecular Biology
Background:
- Renal artery stenosis (RAS) is a significant cause of end-stage renal disease in elderly patients.
- The precise mechanisms underlying RAS-induced renal fibrosis and atrophy remain unclear.
Purpose of the Study:
- To elucidate the mechanisms of renal fibrosis and atrophy in a mouse model of RAS.
- To investigate the roles of peritubular capillary loss, pericyte changes, inflammatory macrophages, and Wnt/β-catenin signaling in RAS.
Main Methods:
- Established a two-kidney, one-clip Goldblatt mouse model.
- Assessed blood pressure, renal morphology, and pathology at multiple time points post-surgery.
- Evaluated peritubular capillary integrity, pericyte behavior, macrophage infiltration, and Wnt/β-catenin signaling.
Main Results:
- RAS led to increased blood pressure, renal atrophy, interstitial fibrosis, and tubular injury.
- Significant peritubular capillary loss and inflammatory macrophage infiltration were observed.
- Pericytes detached from capillaries and migrated, while Wnt/β-catenin signaling was upregulated.
Conclusions:
- Peritubular capillary loss and pericyte alterations are critical in RAS-induced renal fibrosis.
- Inflammatory macrophages and Wnt/β-catenin signaling are implicated in RAS pathology.
- Targeting these pathways may offer therapeutic strategies for preserving renal function in RAS patients.
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