ReviewJournal of biomedicine & biotechnology2012
Involvement of the intrarenal renin-angiotensin system in experimental models of glomerulonephritis.
Review in Journal of biomedicine & biotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Intrarenal renin-angiotensin system activation and macrophage infiltrations in pediatric chronic glomerulonephritis.Pediatric nephrology (Berlin, Germany) · 2023Article
- Foe and friend in the COVID-19-associated acute kidney injury: an insight on intrarenal renin-angiotensin system.Acta biochimica et biophysica Sinica · 2022Review
- Exploring the Underlying Mechanism of Shenyankangfu Tablet in the Treatment of Glomerulonephritis Through Network Pharmacology, Machine Learning, Molecular Docking, and Experimental Validation.Drug design, development and therapy · 2021Article
- Targeting the Wnt/β-Catenin Signaling Pathway as a Potential Therapeutic Strategy in Renal Tubulointerstitial Fibrosis.Frontiers in pharmacology · 2021Review
- Renal Chemerin Expression is Induced in Models of Hypertensive Nephropathy and Glomerulonephritis and Correlates with Markers of Inflammation and Fibrosis.International journal of molecular sciences · 2019Article
- Role of the intrarenal renin-angiotensin system in the progression of renal disease.Pediatric nephrology (Berlin, Germany) · 2017Review
- Deficiency of the Angiotensinase Aminopeptidase A Increases Susceptibility to Glomerular Injury.Journal of the American Society of Nephrology : JASN · 2017Article
- Cardiovascular risk is similar in patients with glomerulonephritis compared to other types of chronic kidney disease: a matched cohort study.BMC nephrology · 2017Article
- Cytosolic Phospholipase A2α Is Essential for Renal Dysfunction and End-Organ Damage Associated With Angiotensin II-Induced Hypertension.American journal of hypertension · 2016Article
- Changes in urinary angiotensinogen posttreatment in pediatric IgA nephropathy patients.Pediatric nephrology (Berlin, Germany) · 2015Article
- Molecular imaging of urogenital diseases.Seminars in nuclear medicine · 2014Review
- Intrarenal renin-angiotensin system in regulation of glomerular function.Current opinion in nephrology and hypertension · 2014Review
- Upregulation of soluble epoxide hydrolase in proximal tubular cells mediated proteinuria-induced renal damage.American journal of physiology. Renal physiology · 2013Article
- STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intrarenal renin-angiotensin system (RAS) has several pathophysiologic functions not only in blood pressure regulation but also in the development of glomerulonephritis (GN). Angiotensin II (Ang II) is the biologically active product of the RAS. Locally produced Ang II induces inflammation, renal cell growth, mitogenesis, apoptosis, migration, and differentiation, regulates the gene expression of bioactive substances, and activates multiple intracellular signaling pathways, leading to tissue damage. Activation of the Ang II type 1 (AT1) receptor pathway results in the production of proinflammatory mediators, cell proliferation, and extracellular matrix synthesis, which facilitates glomerular injury. Previous studies have shown that angiotensin-converting enzyme inhibitors and/or AT1 receptor blockers have beneficial effects in experimental GN models and humans with various types of GN, and that these effects are more significant than their suppressive effects on blood pressure. In this paper, we focus on intrarenal RAS activation in the pathophysiology of experimental models of GN.
Indexed as
Identifiers
What OpenQuestion holds
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.