Evidence map›Paper›PMID 34244467›Full record

ArticleCell death & disease2021

IGF-1 protects against angiotensin II-induced cardiac fibrosis by targeting αSMA.

Sangmi Ock, Woojin Ham, Chae Won Kang, Hyun Kang, Wang Soo Lee, Jaetaek Kim

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  11. Exploring in vivo and in vitro models for heart failure with biomarker insights: a review.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024
    Review
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  16. Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023
    Article
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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 1 institution in 1 country.

Sangmi OckDivision of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.
Woojin HamDivision of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.
Chae Won KangDivision of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.
Hyun KangDepartment of Anesthesiology, College of Medicine, Chung-Ang University, Seoul, Korea.
Wang Soo LeeDivision of Cardiology, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea. wslee1227@cau.ac.kr.
Jaetaek KimDivision of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea. jtkim@cau.ac.kr.
Chung-Ang University · KR

Funding

National Research Foundation of Korea (NRF) 2020R1A2C1009647National Research Foundation of Korea (NRF) 2020R1A2C1010217
6 · The paper itself

Abstract

The insulin-like growth factor 1 receptor (IGF-1R) signaling in cardiomyocytes is implicated in physiological hypertrophy and myocardial aging. Although fibroblasts account for a small amount of the heart, they are activated when the heart is damaged to promote cardiac remodeling. However, the role of IGF-1R signaling in cardiac fibroblasts is still unknown. In this study, we investigated the roles of IGF-1 signaling during agonist-induced cardiac fibrosis and evaluated the molecular mechanisms in cultured cardiac fibroblasts. Using an experimental model of cardiac fibrosis with angiotensin II/phenylephrine (AngII/PE) infusion, we found severe interstitial fibrosis in the AngII/PE infused myofibroblast-specific IGF-1R knockout mice compared to the wild-type mice. In contrast, low-dose IGF-1 infusion markedly attenuated AngII-induced cardiac fibrosis by inhibiting fibroblast proliferation and differentiation. Mechanistically, we demonstrated that IGF-1-attenuated AngII-induced cardiac fibrosis through the Akt pathway and through suppression of rho-associated coiled-coil containing kinases (ROCK)2-mediated α-smooth muscle actin (αSMA) expression. Our study highlights a novel function of the IGF-1/IGF-1R signaling in agonist-induced cardiac fibrosis. We propose that low-dose IGF-1 may be an efficacious therapeutic avenue against cardiac fibrosis.

Indexed as

ActinsAngiotensin IIAnimalsCardiomyopathiesCell ProliferationCells, CulturedDisease Models, AnimalFibroblastsFibrosisInfusions, IntravenousInsulin-Like Growth Factor IMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacActinsalpha-smooth muscle actin, mouseAngiotensin IIIgf1r protein, mouseInsulin-Like Growth Factor IPhenylephrineProto-Oncogene Proteins c-aktReceptor, IGF Type 1rho-Associated KinasesRock2 protein, mouse

Identifiers

PMID34244467
PMCPMC8270920
OpenAlexW3177551097

What OpenQuestion holds

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LicenceCC BY
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.