ReviewInternational journal of molecular sciences2023
Non-Haemodynamic Mechanisms Underlying Hypertension-Associated Damage in Target Kidney Components.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Metabolomics and Precision Medicine in Resistant Hypertension: Pathophysiological Insights, Biomarker Discovery, and Translational Strategies.International journal of hypertension · 2026Review
- Blood pressure control after solid organ transplantation: opportunities for optimizing care.Transplant international : official journal of the European Society for Organ Transplantation · 2026Article
- Body Mass Index as a Potential Mediator of the Association Between Gout and Hypertension Among Chinese Older Adults: A Mediation Analysis in a Cross-Sectional Study.Aging medicine (Milton (N.S.W)) · 2025Article
- Nephroprotective Mechanisms of SGLT2i: Beyond the Glucose-Lowering Effect.Biomedicines · 2025Review
- Beyond Blood Pressure: Emerging Pathways and Precision Approaches in Hypertension-Induced Kidney Damage.International journal of molecular sciences · 2025Review
- Insights into renal damage in hyperuricemia: Focus on renal protection (Review).Molecular medicine reports · 2025Review
- Estimated pulse wave velocity as a potential predictor of albuminuria in hypertension.Frontiers in medicine · 2025Article
- HIF-1α knockdown attenuates phenotypic transformation and oxidative stress induced by high salt in human aortic vascular smooth muscle cells.Scientific reports · 2024Article
- Hypotensive and Cardioprotective Potential of Yellow Bedstraw Extract-Based Oral Liquid in Spontaneously Hypertensive Rats.International journal of molecular sciences · 2024Article
- The Renoprotective Mechanisms of Sodium-Glucose Cotransporter-2 Inhibitors (SGLT2i)-A Narrative Review.International journal of molecular sciences · 2024Review
- A Comment on 'Clinical Value of Urinary Wilms' Tumour-1 and Mu-Glutathione S-Transferase Gene Expression in Kidney Injury in Type 2 Diabetes Mellitus: Important Considerations for Clinical Application' [Letter].Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Novel Insights into the Molecular Mechanisms of Atherosclerosis.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arterial hypertension (AH) is a global challenge that greatly impacts cardiovascular morbidity and mortality worldwide. AH is a major risk factor for the development and progression of kidney disease. Several antihypertensive treatment options are already available to counteract the progression of kidney disease. Despite the implementation of the clinical use of renin-angiotensin aldosterone system (RAAS) inhibitors, gliflozins, endothelin receptor antagonists, and their combination, the kidney damage associated with AH is far from being resolved. Fortunately, recent studies on the molecular mechanisms of AH-induced kidney damage have identified novel potential therapeutic targets. Several pathophysiologic pathways have been shown to play a key role in AH-induced kidney damage, including inappropriate tissue activation of the RAAS and immunity system, leading to oxidative stress and inflammation. Moreover, the intracellular effects of increased uric acid and cell phenotype transition showed their link with changes in kidney structure in the early phase of AH. Emerging therapies targeting novel disease mechanisms could provide powerful approaches for hypertensive nephropathy management in the future. In this review, we would like to focus on the interactions of pathways linking the molecular consequences of AH to kidney damage, suggesting how old and new therapies could aim to protect the kidney.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.