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Hypertension-Induced Renal Injury: From Pathophysiology to Therapeutic Perspectives
Ning Zhou1, Su-Ye Zhong1, Pan Gao1
1Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Biomedicines
|March 28, 2026
Summary
Hypertension damages kidneys through molecular pathways, not just blood pressure. Understanding early endothelial dysfunction and hypoxia is key to developing new treatments for chronic kidney disease.
Area of Science:
- Nephrology
- Cardiovascular Research
- Molecular Medicine
Background:
- Hypertension is a leading cause of chronic kidney disease (CKD) and end-stage renal disease.
- Kidney injury in hypertension involves complex molecular mechanisms beyond hemodynamic stress.
Purpose of the Study:
- To present a network-based framework integrating molecular insights into hypertension-induced renal injury.
- To highlight critical early events and amplifying pathways driving disease progression.
- To discuss diagnostic biomarkers and therapeutic strategies for renoprotection.
Main Methods:
- Systematic review and integration of current mechanistic data.
- Network-based and stage-structured framework development.
- Analysis of molecular pathways, including RAAS, oxidative stress, inflammation, and fibrosis.
Main Results:
- Early endothelial dysfunction and renal hypoxia create a permissive environment for injury.
- Amplifying pathways (RAAS, oxidative stress, inflammation, SNS) interact via feedback loops.
- Fibrotic programs (EMT, fibroblast activation) lead to irreversible damage; epigenetics, gut-kidney axis, autophagy, and aging also contribute.
Conclusions:
- An 'early-window' of endothelial dysfunction and hypoxia is critical.
- Interplay between amplifying mechanisms explains therapeutic resistance.
- Integrating molecular insights enables early detection and precision intervention for hypertension-induced renal injury.
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