ReviewClinical and experimental nephrology2015
The biological significance of angiotensin-converting enzyme inhibition to combat kidney fibrosis.
Review in Clinical and experimental nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis.International journal of molecular sciences · 2022Review
- More than just an enzyme: Dipeptidyl peptidase-4 (DPP-4) and its association with diabetic kidney remodelling.Pharmacological research · 2019Review
- Oral Administration of N-Acetyl-seryl-aspartyl-lysyl-proline Ameliorates Kidney Disease in Both Type 1 and Type 2 Diabetic Mice via a Therapeutic Regimen.BioMed research international · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both angiotensin-converting enzyme inhibitor (ACE-I) and angiotensin II receptor blocker have been recognized as renin-angiotensin system (RAS) inhibitors. These two RAS inhibitors are rarely recognized as drugs with distinct pharmacological effects in the clinic or most clinical trials. Some preclinical basic research and clinical trials indicate that ACE-I might display superior organ-protective effects, especially anti-fibrotic effects. Such anti-fibrotic effects of ACE-I could be associated with an endogenous anti-fibrotic peptide, N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). In this review, we focused on the anti-fibrotic effects of RAS inhibition and the endogenous anti-fibrotic peptide AcSDKP.
Indexed as
Identifiers
24975544What 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.