ArticleJournal of molecular histology2025
The role of AT-1 antagonist on wound healing in rats with hypertension and diabetes.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Pathogenesis of Neovascular Glaucoma in Diabetic Retinopathy: A Review.Journal of ophthalmology · 2026Review
- Article
- Beyond blood pressure: the renin-angiotensin system as an innovative driver and therapeutic target in pathological scarring.Frontiers in pharmacology · 2026Review
- An Agonist of Zinc-Sensing G-Protein Coupled Receptor 39 Accelerates Skin Wound Healing and Protects Against UVB-Induced Keratinocyte Damage.Journal of experimental pharmacology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Wound healing is a complex process involving molecular and structural interactions. Transforming growth factor β (TGF-β), the renin-angiotensin system (RAS), and other important mediators play a central role on wound healing process. This study examined the dynamics of healing in healthy, hypertensive, and diabetic rats treated with or without Losartan, focusing on healing rate, scar characteristics, and molecular modulation. Macroscopic and microscopic analyses revealed delayed healing and reduced collagen deposition in diabetic and hypertensive rats compared with normoglycemic controls. Losartan affected healing by regulating TGF-β expression and collagen organization. In the groups of hypertensive and diabetic rats treated with losartan, healing aesthetics improved by less collagen deposition and consequently minor chances to fibrosis development, probably due to lower TGFβ and SMADs expression. Diabetic rats showed reduced skin and collagen fiber thickness, whereas hypertensive rats showed better healing under Losartan treatment (LT). These results demonstrate the complex interactions between LT, diabetes and hypertension on important fibrotic and inflammatory pathways. Although LT successfully reduces TGF-β expression and classical SMAD signaling in hypertensive settings, its minor effect in diabetes conditions indicate the necessity of supplemental treatments that target mechanisms unique to hyperglycemia, such as glycation end products or oxidative stress inhibitors. To improve treatment outcomes for individuals with diabetes and hypertension comorbidities, future studies should investigate the combination of multi-pathway modulators.
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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.