ArticleJournal of the American Society of Nephrology : JASN2012
Liver angiotensinogen is the primary source of renal angiotensin II.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
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Who cites it
154 citing papers in PubMed, 270 citations in OpenAlex.
- Trial
- Differential serum dynamics of apelin, elabela, and angiotensinogen in CKD and haemodialysis: insights into peptide modulation across the dialysis procedure.Renal failure · 2026Article
- Upregulation of angiotensin-(1-7) formation in human podocytes - enzyme activity assay upon fluid flow shear stress.PloS one · 2026Article
- Loss of the liver circadian clock affects the expression of intrarenal renin-angiotensin system components.Scientific reports · 2025Article
- The relationship between estrogen and renin angiotensin system components in the context of hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Review
- Loss of Hepatic Angiotensinogen Attenuates Diastolic Dysfunction in Heart Failure with Preserved Ejection Fraction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A novel glomerulopathy model demonstrates renal counterbalance via local angiotensin II regulation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025Article
- Keratinocyte-specific angiotensin II receptor-associated protein deficiency exacerbates angiotensin II-dependent hypertension via activation of the skin renin-angiotensin system.Nature communications · 2025Article
- Article
- Novel Antihypertensive Medications to Target the Renin-Angiotensin System: Mechanisms and Research.Reviews in cardiovascular medicine · 2025Review
- Acute kidney injury recovery status predicts mortality and cardiorenal outcomes in patients admitted with acute decompensated heart failure.Open heart · 2025Observational
- Hepatocyte-specific angiotensinogen deficiency inhibits Western diet-induced liver steatosis with suppression of cell division in mice.Global translational medicine · 2025Article
- Renal Proximal Tubule Cell-Specific Megalin Deletion Does Not Affect Atherosclerosis But Induces Tubulointerstitial Nephritis in Mice Fed a Western Diet.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Exploratory Studies on RNAi-Based Therapies Targeting Angiotensinogen in Hypertension: Scoping Review.Journal of personalized medicine · 2024Review
- An organotypic atlas of human vascular cells.Nature medicine · 2024Article
- Renal Proximal Tubule Cell-specific Megalin Deletion Does Not Affect Atherosclerosis But Induces Tubulointerstitial Nephritis in Mice Fed Western Diet.bioRxiv : the preprint server for biology · 2024Article
- Emerging Trends and Innovations in the Treatment and Diagnosis of Atherosclerosis and Cardiovascular Disease: A Comprehensive Review towards Healthier Aging.Pharmaceutics · 2024Review
- Review
- Angiotensinogen as a Therapeutic Target for Cardiovascular and Metabolic Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Article
94 more citing papers are in PubMed but not listed here.
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8 authors at 5 institutions in 2 countries.
Funding
Abstract
Angiotensin II content in the kidney is much higher than in the plasma, and it increases more in kidney diseases through an uncertain mechanism. Because the kidney abundantly expresses angiotensinogen mRNA, transcriptional dysregulation of angiotensinogen within the kidney is one potential cause of increased renal angiotensin II in the setting of disease. Here, we observed that kidney-specific angiotensinogen knockout mice had levels of renal angiotensinogen protein and angiotensin II that were similar to those levels of control mice. In contrast, liver-specific knockout of angiotensinogen nearly abolished plasma and renal angiotensinogen protein and renal tissue angiotensin II. Immunohistochemical analysis in mosaic proximal tubules of megalin knockout mice revealed that angiotensinogen protein was incorporated selectively in megalin-intact cells of the proximal tubule, indicating that the proximal tubule reabsorbs filtered angiotensinogen through megalin. Disruption of the filtration barrier in a transgenic mouse model of podocyte-selective injury increased renal angiotensin II content and markedly increased both tubular and urinary angiotensinogen protein without an increase in renal renin activity, supporting the dependency of renal angiotensin II generation on filtered angiotensinogen. Taken together, these data suggest that liver-derived angiotensinogen is the primary source of renal angiotensinogen protein and angiotensin II. Furthermore, an abnormal increase in the permeability of the glomerular capillary wall to angiotensinogen, which characterizes proteinuric kidney diseases, enhances the synthesis of renal angiotensin II.
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