ArticleMolecular medicine reports2017
The ACE2-Ang (1-7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Overexpression of angiotensin-converting enzyme 2 by renin-angiotensin system inhibitors. Truth or myth? A systematic review of animal studies.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Pooled it
- Mas receptor activation regulates the functional phenotype of myocardial macrophages through the Akt/Nrf2 signaling pathway to alleviate sepsis-induced cardiomyopathy.Journal of translational medicine · 2026Article
- ACE/ACE2 axis in cardiovascular disease and COVID-19: Molecular insights and therapeutic perspectives.Journal of cardiovascular and thoracic research · 2026Review
- A novel angiotensin(1-7) agonist, PNA5, reduces ischemic reperfusion injury and cardiac dysfunction.Frontiers in cardiovascular medicine · 2026Article
- Unlocking Novel Therapeutic Potential of Angiotensin II Receptor Blockers.International journal of molecular sciences · 2025Review
- Serum Ang 1, Ang 1-7, and Mas levels as potential biomarkers in obstructive sleep apnea syndrome.Biomarkers in medicine · 2025Article
- Lnc PVT1 facilitates TGF-β1-induced human cardiac fibroblast activation in vitro and ISO-induced myocardial fibrosis in vivo through regulating MYC.Molecular and cellular biochemistry · 2025Article
- Angiotensin-(1-7) Inhibits Angiogenesis and Alleviates Joint Damage in CIA Mice via the Hippo-YAP Pathway.Journal of inflammation research · 2025Article
- Research progress on the natural products in the intervention of myocardial infarction.Frontiers in pharmacology · 2024Review
- Myocardial Angiotensin-Converting Enzyme 2 Protein Expression in Ischemic Heart Failure.International journal of molecular sciences · 2023Article
- PDZK1 improves ventricular remodeling in hypertensive rats by regulating the stability of the Mas receptor.Amino acids · 2023Article
- Ameliorative effect of mussel-derived ACE inhibitory peptides on spontaneous hypertension rats.European journal of nutrition · 2023Article
- Serum levels of angiotensin-converting enzyme 2 in children with Kawasaki disease.Clinical and experimental medicine · 2023Article
- COVID-19-Induced Myocarditis: Pathophysiological Roles of ACE2 and Toll-like Receptors.International journal of molecular sciences · 2023Review
- Angiotensin II Type 1 Receptor Blocker Prevents Abdominal Aortic Aneurysm Progression in Osteoprotegerin-Deficient Mice via Upregulation of Angiotensin (1-7).Journal of the American Heart Association · 2023Article
- Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis.International journal of molecular sciences · 2023Review
- Inappropriate activation of the renin-angiotensin system improves cardiac tolerance to ischemia/reperfusion injury in rats with late angiotensin II-dependent hypertension.Frontiers in physiology · 2023Article
- Alamandine alleviated heart failure and fibrosis in myocardial infarction mice.Biology direct · 2022Article
- Insights into Cardiovascular Defects and Cardiac Epigenome in the Context of COVID-19.Epigenomes · 2022Review
- The miR-214-3p/c-Ski axis modulates endothelial-mesenchymal transition in human coronary artery endothelial cells in vitro and in mice model in vivo.Human cell · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial remodeling serves an important role in the pathophysiology of coronary heart disease. The angiotensin-converting enzyme (ACE)2-angiotensin-(1-7) [Ang (1‑7)]‑Mas receptor (MasR) axis is a key regulator in myocardial remodeling and development of heart failure. To investigate how ACE2‑Ang‑(1‑7)‑MasR axis function on myocardial remodeling and cardiac fibrosis in post‑myocardial infarction (MI), male Sprague‑Dawley rats (weight, 200±20 g) were used to establish the model of myocardial infarction by ligating the left coronary artery. The present study suggests that telmisartan (Tel) and olmesartan (Olm) (5 mg/kg/d) can inhibit myocardial remodeling of post‑myocardial infarction through the ACE2‑Ang (1‑7)‑MasR pathway. Administration of Tel or Olm was demonstrated to significantly inhibit collagen deposition using Masson staining. In addition, telmisartan and olmesartan was indicated to antagonize angiotensin II (Ang II) and upregulate ACE2, MasR, Ang (1‑7) expression in myocardial tissue using immunoassay and ELISA test, and the effect of Olm was more marked than that of Tel at the same dosage. Simultaneously, compared with the MI or Sham group, the mRNA and protein expression of ACE2, Ang II and MasR in myocardial tissue demonstrated a remarkable increase in the Olm group, when compared with the Tel group. Taken together, our data demonstrated that ACE2‑Ang (1‑7)‑MasR axis may present a potential protective role in the development of myocardial remodeling and may provide a new target for drug development of cardiac fibrosis. In conclusion, Olm is superior to Tel in inhibiting myocardial local Ang II level reducing myocardial collagen deposition and improving myocardial remodeling by upregulating the expression of ACE2, Ang (1‑7) and MasR.
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.