The Role of Non-Coding RNA in the Pathogenesis of Hypertensive Nephropathy.
Cells 2026 Apr 15; 15(8).

Abstract

Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease and end-stage renal disease worldwide and results from the long-term effects of hypertension on renal structure and function. The pathogenesis of HN is complex and involves haemodynamic disturbances, renal vascular injury, oxidative stress, chronic inflammation, and progressive interstitial fibrosis. In recent years, increasing attention has focused on the role of non-coding RNAs (ncRNAs)-including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs)-as key regulators of gene expression involved in these processes. This review summarises the current understanding of the molecular mechanisms underlying HN, with particular emphasis on the roles of oxidative stress, activation of the renin-angiotensin-aldosterone system, transforming growth factor beta signalling, and inflammatory and fibrogenic pathways. The contribution of dysregulated ncRNAs to endothelial dysfunction, inflammatory responses, apoptosis, angiogenesis, and renal remodelling and fibrosis is also discussed. Particular attention is given to miRNAs and lncRNAs as mediators of disease progression and potential biomarkers, as well as to the emerging role of circRNAs in hypertensive kidney injury, including their involvement in the regulation of redox balance and intercellular communication. Collectively, available evidence indicates that ncRNAs represent a critical link between haemodynamic stimuli and persistent molecular alterations in renal tissue, highlighting their potential as diagnostic markers and therapeutic targets in HN.

Authors+Show Affiliations

Plewa P0009-0008-6821-0086Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Figiel KDepartment of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Ćmil M0009-0000-1594-5646Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Skórka P0009-0006-6080-6104Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Kupis KDepartment of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Pawlik A0000-0001-6557-1208Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

42041569