Evidence map›Paper›PMID 28447738›Full record

ArticleMolecular medicine reports2017

Telmisartan suppresses cardiac hypertrophy by inhibiting cardiomyocyte apoptosis via the NFAT/ANP/BNP signaling pathway.

Xiurong Li, Yuhuai Lan, Yan Wang, Minghao Nie, Yanhong Lu, Eryang Zhao

Open access · hybridAbstract read
In one paragraph

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 44 citations in OpenAlex.

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  16. [Rosmarinic acid inhibits high glucose-induced cardiomyocyte hypertrophy by activating Parkin-mediated mitophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Xiurong LiDepartment of Pathology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China.
Yuhuai LanIntensive Care Unit, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China.
Yan WangDepartment of Pathology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China.
Minghao NieDepartment of Pathology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China.
Yanhong LuDepartment of Pathology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China.
Eryang ZhaoDepartment of Oral Pathology, Stomatological Hospital, Harbin Medical University, Harbin, Heilongjiang 150036, P.R. China.
Heilongjiang Provincial Hospital · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telmisartan, a type of angiotensin II (Ang II) receptor inhibitor, is a common agent used to treat hypertension in the clinic. Hypertension increases cardiac afterload and promotes cardiac hypertrophy. However, the ventricular Ang II receptor may be activated in the absence of hypertension. Therefore, telmisartan may reduce cardiac hypertrophy by indirectly ameliorating hypertensive symptoms and directly inhibiting the cardiac Ang II receptor. Nuclear factor of activated T‑cells (NFAT) contributes to cardiac hypertrophy via nuclear translocation, which induces a cascade of atrial natriuretic peptide (ANP) and brain/B‑type natriuretic peptide (BNP) expression and cardiomyocyte apoptosis. However, NFAT-mediated inhibition of cardiac hypertrophy by telmisartan remains poorly understood. The present study demonstrated that telmisartan suppressed cardiomyocyte hypertrophy in a mouse model of cardiac afterload and in cultured cardiomyocytes by inhibiting NFAT nuclear translocation, as well as by inhibiting ANP and BNP expression and cardiomyocyte apoptosis, in a dose‑dependent manner. The present study provides a novel insight into the potential underlying mechanisms of telmisartan-induced inhibition of cardiomyocyte hypertrophy, which involves inhibition of NFAT activation, nuclear translocation and the ANP/BNP cascade.

Indexed as

Active Transport, Cell NucleusAnimalsApoptosisAtrial Natriuretic FactorBenzimidazolesBenzoatesCardiomegalyCell NucleusMaleMiceMyocytes, CardiacNatriuretic Peptide, BrainNFATC Transcription FactorsSignal TransductionTelmisartanAtrial Natriuretic FactorBenzimidazolesBenzoatesNatriuretic Peptide, BrainNFATC Transcription FactorsTelmisartan

Identifiers

PMID28447738
PMCPMC5428554
OpenAlexW2601633584

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.