ArticleAmerican journal of physiology. Renal physiology2015
Antisense-mediated angiotensinogen inhibition slows polycystic kidney disease in mice with a targeted mutation in Pkd2.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Design of Nanocarriers for Kidney Targeted Delivery of Nucleic Acid Therapeutics.Macromolecular bioscience · 2026Review
- The Versatile Applications of Antisense Oligonucleotides in Modern Medicine.International journal of molecular sciences · 2026Review
- RNA-based therapeutic opportunities for the treatment of kidney diseases.Nature reviews. Nephrology · 2026Review
- Targeting a pathogenic cryptic exon that drives HLRCC to induce exon skipping.Molecular therapy. Nucleic acids · 2025Article
- RNA-Based Therapies in Kidney Diseases.Journal of inflammation research · 2025Review
- Gene therapy and kidney diseases.Molecular therapy. Methods & clinical development · 2024Review
- Raising serum uric acid with a uricase inhibitor worsens PKD in rat and mouse models.American journal of physiology. Renal physiology · 2024Article
- New Approaches Targeting the Renin-Angiotensin System: Inhibition of Brain Aminopeptidase A, ACE2 Ubiquitination, and Angiotensinogen.The Canadian journal of cardiology · 2023Review
- Does the Naked Emperor Parable Apply to Current Perceptions of the Contribution of Renin Angiotensin System Inhibition in Hypertension?Current hypertension reports · 2022Review
- Immunoneutralization of human angiotensin-(1-12) with a monoclonal antibody in a humanized model of hypertension.Peptides · 2022Article
- The Angiotensin-(1-12)/Chymase axis as an alternate component of the tissue renin angiotensin system.Molecular and cellular endocrinology · 2021Review
- Oligonucleotide-Based Therapies for Renal Diseases.Biomedicines · 2021Review
- Metabolic Reprogramming and Reconstruction: Integration of Experimental and Computational Studies to Set the Path Forward in ADPKD.Frontiers in medicine · 2021Review
- STAT signaling in polycystic kidney disease.Cellular signalling · 2020Review
- The pathogenic AGT c.856+1G>T mutation of a patient with multiple renal cysts and hypertension.Annals of translational medicine · 2019Article
- Novel Therapeutic Approaches Targeting the Renin-Angiotensin System and Associated Peptides in Hypertension and Heart Failure.Pharmacological reviews · 2019Review
- Antisense oligonucleotides targeting angiotensinogen: insights from animal studies.Bioscience reports · 2019Review
- Emerging targeted strategies for the treatment of autosomal dominant polycystic kidney disease.Clinical kidney journal · 2018Review
- Precision gene editing technology and applications in nephrology.Nature reviews. Nephrology · 2018Review
- Proteomic analysis of AQP11-null kidney: Proximal tubular type polycystic kidney disease.Biochemistry and biophysics reports · 2018Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Renal cyst enlargement is associated with the activation of both the circulating and intrarenal renin-angiotensin systems. Angiotensinogen (AGT) is the substrate for renin. The aim of the present study was to determine the effect of AGT inhibition on renal cyst enlargement. An AGT antisense oligonucleotide (ASO) that selectively inhibits AGT mRNA was injected once weekly in PKD2WS25 mice [an orthologous model of human autosmal dominant polycystic kidney disease (PKD) involving mutation of the Pkd2 gene] from 4 to 16 wk of age. The AGT ASO resulted in a 40% decrease in AGT RNA in the kidney, a 60% decrease in AGT RNA in the liver, and a significant decrease in AGT protein in the kidney and serum. The AGT ASO resulted in a significant decrease in kidney size, cyst volume density, and blood urea nitrogen. The AGT ASO resulted in a significant decrease in transforming growth factor-β and interstitial fibrosis in the kidney. Mice treated with the AGT ASO had a significant decrease in proinflammatory cytokines [chemokine (C-X-C motif) ligand (CXCL)1 and IL-12] in the kidney. Cluster of differentiation (CD)36 is a scavenger receptor found on tubular cells that can activate the renin-angiotensin system. Administration of a CD36 ASO had no effect on PKD and kidney function, suggesting that the effect of the AGT ASO is independent of CD36. In summary, AGT inhibition resulted in significant decreases in kidney size and cyst volume and an improvement in kidney function in PKD mice. The AGT ASO resulted in a decrease in transforming growth factor-β, interstitial fibrosis, and the proinflammatory cytokines CXCL1 and IL-12 in the kidney.
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