ArticleHypertension (Dallas, Tex. : 1979)2015
Elevated Endothelial Hypoxia-Inducible Factor-1α Contributes to Glomerular Injury and Promotes Hypertensive Chronic Kidney Disease.
Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
- Hypertension-Induced Renal Injury: From Pathophysiology to Therapeutic Perspectives.Biomedicines · 2026Review
- A Machine Learning Method for Predicting Acute Kidney Injury in Patients with Intracranial Hemorrhage.Cell biochemistry and biophysics · 2025Article
- The gut-kidney axis in high-altitude hypoxia: pathophysiological mechanisms and the central role of hypoxia inducible factor.Annals of medicine · 2025Review
- Characteristics and Outcomes of IgA Nephropathy Patients With SGLT2 Inhibitor-Induced Polycythemia.Cureus · 2025Article
- Moderate intensity continuous training mitigates hypertension-induced renal fibrosis by inhibiting HIF-1α-mediated autophagy.Frontiers in physiology · 2025Article
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- Hypoxia-inducible factors and essential hypertension: narrative review of experimental and clinical data.Pharmacological reports : PR · 2023Review
- No benefit of HIF prolyl hydroxylase inhibition for hypertensive renal damage in renovascular hypertensive rats.Frontiers in physiology · 2023Article
- Hypoxia-inducible factor signaling in vascular calcification in chronic kidney disease patients.Journal of nephrology · 2022Review
- Pathological Connections between Nonalcoholic Fatty Liver Disease and Chronic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2022Review
- Hypoxia-Inducible Factors and Diabetic Kidney Disease-How Deep Can We Go?International journal of molecular sciences · 2022Review
- Role of hypoxia preconditioning in therapeutic potential of mesenchymal stem-cell-derived extracellular vesicles.World journal of stem cells · 2022Review
- TIGAR deficiency sensitizes angiotensin-II-induced renal fibrosis and glomerular injury.Physiological reports · 2022Article
- Erythrocyte transglutaminase-2 combats hypoxia and chronic kidney disease by promoting oxygen delivery and carnitine homeostasis.Cell metabolism · 2022Article
- Coassembly of hypoxia-sensitive macrocyclic amphiphiles and extracellular vesicles for targeted kidney injury imaging and therapy.Journal of nanobiotechnology · 2021Article
- Intratubular, Intracellular, and Mitochondrial Angiotensin II/ATFrontiers in physiology · 2021Review
- Sodium-Glucose Cotransporter 2 Inhibitors Work as a "Regulator" of Autophagic Activity in Overnutrition Diseases.Frontiers in pharmacology · 2021Review
- Qian Yang Yu Yin Granule Improves Renal Injury of Hypertension by Regulating Metabolic Reprogramming Mediated by HIF-1α/PKM2 Positive Feedback Loop.Frontiers in pharmacology · 2021Article
- Pathogenesis and Damage Targets of Hypertensive Kidney Injury.Journal of translational internal medicine · 2020Article
- Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Hypertensive chronic kidney disease is one of the most prevalent medical conditions with high morbidity and mortality in the United States and worldwide. However, early events initiating the progression to hypertensive chronic kidney disease are poorly understood. We hypothesized that elevated endothelial hypoxia-inducible factor-1α (HIF-1α) is a common early insult triggering initial glomerular injury leading to hypertensive chronic kidney disease. To test our hypothesis, we used an angiotensin II infusion model of hypertensive chronic kidney disease to determine the specific cell type and mechanisms responsible for elevation of HIF-1α and its role in the progression of hypertensive chronic kidney disease. Genetic studies coupled with reverse transcription polymerase chain reaction profiling revealed that elevated endothelial HIF-1α is essential to initiate glomerular injury and progression to renal fibrosis by the transcriptional activation of genes encoding multiple vasoactive proteins. Mechanistically, we found that endothelial HIF-1α gene expression was induced by angiotensin II in a nuclear factor-κB-dependent manner. Finally, we discovered reciprocal positive transcriptional regulation of endothelial Hif-1α and Nf-κb genes is a key driving force for their persistent activation and disease progression. Overall, our findings revealed that the stimulation of HIF-1α gene expression in endothelial cells is detrimental to induce kidney injury, hypertension, and disease progression. Our findings highlight early diagnostic opportunities and therapeutic approaches for hypertensive chronic kidney disease.
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Registered trials
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