Evidence map›Paper›PMID 34631707›Full record

ArticleFrontiers in cell and developmental biology2021

Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses.

Gabriel Komla Adzika, Hongjian Hou, Adebayo Oluwafemi Adekunle, Ruqayya Rizvi, Seyram Yao Adzraku, Kexue Li, Qi-Ming Deng, Richard Mprah, Marie Louise Ndzie Noah, Joseph Adu-Amankwaah and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

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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

16 authors at 5 institutions in 3 countries.

Gabriel Komla AdzikaDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Hongjian HouDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Adebayo Oluwafemi AdekunleDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Ruqayya RizviXuzhou Medical University, Xuzhou, China.
Seyram Yao AdzrakuKey Laboratory of Bone Marrow Stem Cell, Department of Hematology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Kexue LiDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Qi-Ming DengThe Key Laboratory of Cardiovascular Remodeling and Function Research, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Chinese Ministry of Education, Department of Cardiology, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, China.
Richard MprahDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Marie Louise Ndzie NoahDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Joseph Adu-AmankwaahDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Jeremiah Ong'achwa MachukiDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Wenkang ShangFaculty of Biology, Institute of Biochemistry and Molecular Biology, ZBMZ, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
Tongtong MaDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Stephane KodaLaboratory of Infection and Immunity, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Xuzhou, China.
Xianluo MaInternal Medicine-Cardiovascular Department, People's Hospital of Jiawang District, Xuzhou, China.
Hong SunDepartment of Physiology, Xuzhou Medical University, Xuzhou, China.
Xuzhou Medical College · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShangqiu Normal University · CNUniversity of Freiburg · DEXuzhou No.1 People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic catecholamine stress (CCS) induces the occurrence of cardiomyopathy-pathological cardiac hypertrophy (PCH), which is characterized by left ventricular systolic dysfunction (LVSD). Recently, mounting evidence has implicated myocardial inflammation in the exacerbation of pathological cardiac remodeling. However, there are currently no well-defined treatment interventions or regimes targeted at both the attenuation of maladaptive myocardial hypertrophy and inflammation during CCS to prevent PCH. G protein-coupled receptor kinase 5 (GRK5) and adenylyl cyclases (ACs)-cAMP mediates both cardiac and inflammatory responses. Also, GRK5 and ACs are implicated in stress-induced LVSD. Herein, we aimed at preventing PCH during CCS via modulating adaptive cardiac and inflammatory responses by inhibiting GRK5 and/or stimulating ACs. Isoproterenol-induced cardiomyopathy (ICM) was modeled using 0.5 mg/100 g/day isoproterenol injections for 40 days. Alterations in cardiac and inflammatory responses were assessed from the myocardia. Similarities in the immunogenicity of cardiac troponin I (cTnI) and lipopolysaccharide under CCS were assessed, and Amlexanox (35 μM/ml) and/or Forskolin (10 μM/ml) were then employed

Indexed as

adenylyl cyclaseamlexanoxcAMPchronic catecholamine stressforskolinGRK5inflammationisoproterenol-induced cardiomyopathy

Identifiers

PMID34631707
PMCPMC8497899
OpenAlexW3201723581

What OpenQuestion holds

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Registered trials

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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.