ArticleExperimental and therapeutic medicine2015
Effects of angiotensin II on transient receptor potential melastatin 7 channel function in cardiac fibroblasts.
Article in Experimental and therapeutic medicine, 2015. 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, 19 citations in OpenAlex.
- Calcium Signaling in Cardiac Fibroblasts: Roles in Fibrosis and Therapeutic Implications.Cardiovascular drugs and therapy · 2026Review
- CaBiomedicines · 2025Review
- Progress on role of ion channels of cardiac fibroblasts in fibrosis.Frontiers in physiology · 2023Review
- Magnesium in renal fibrosis.International urology and nephrology · 2022Review
- Emerging role of transient receptor potential (TRP) ion channels in cardiac fibroblast pathophysiology.Frontiers in physiology · 2022Review
- Role of TRPM7 in cardiac fibrosis: A potential therapeutic target (Review).Experimental and therapeutic medicine · 2021Review
- Roles of Biomarkers in Myocardial Fibrosis.Aging and disease · 2020Review
- Mapping TRPM7 Function by NS8593.International journal of molecular sciences · 2020Review
- CaJournal of cardiovascular development and disease · 2019Review
- Transient receptor potential channels in cardiac health and disease.Nature reviews. Cardiology · 2019Review
- TRP Channels Mediated Pathological CaFrontiers in cardiovascular medicine · 2019Review
- TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling.Frontiers in physiology · 2019Review
- Naringenin inhibits transforming growth factor-β1-induced cardiac fibroblast proliferation and collagen synthesis via G0/G1 arrest.Experimental and therapeutic medicine · 2017Article
- A peptide vaccine targeting angiotensin II attenuates the cardiac dysfunction induced by myocardial infarction.Scientific reports · 2017Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the electrophysiological properties of transient receptor potential melastatin 7 (TRPM7) channels in the cell membranes of cardiac fibroblasts (CFs). CFs obtained from Sprague-Dawley rats were treated with six different concentrations of angiotensin (Ang) II for 12 h. The optimum concentration of Ang II for inducing fibrosis was selected by measuring collagen protein expression levels at each concentration. The optimum concentration of Ang II was then used to treat the CFs at five different time-points, and the TRPM7 current across the CF membranes was recorded along with the collagen protein levels in each group. The optimum Ang II concentration for inducing fibrosis was found to be 1 nmol/l; when it was administered to CFs at 0, 6, 12, 24 and 48 h, the protein expression levels of TRPM7 and collagen III initially increased, reaching maximum levels at 12 h, and then decreased. This result positively correlated with the TRPM7 current levels on either side of the CF membranes: The TRPM7 current under the effect of the optimal Ang II concentration for inducing fibrosis was initially increased and then later decreased. This is one of the key mechanisms by which Ang II mediates the proliferation and apoptosis of CFs. This knowledge may be used to identify treatments for the prevention of cardiac fibrosis.
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.