Evidence map›Paper›PMID 33524540›Full record

ArticlePharmacological research2021

Resistin induces cardiac fibroblast-myofibroblast differentiation through JAK/STAT3 and JNK/c-Jun signaling.

Rajvir Singh, Ravinder K Kaundal, Baoyin Zhao, Rihab Bouchareb, Djamel Lebeche

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pharmacological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.3field-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

52 citing papers in PubMed, 77 citations in OpenAlex.

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  12. Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026
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  19. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
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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

5 authors at 1 institution in 1 country.

Rajvir SinghCardiovascular Research Institute, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Ravinder K KaundalCardiovascular Research Institute, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Baoyin ZhaoCardiovascular Research Institute, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Rihab BoucharebCardiovascular Research Institute, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Djamel LebecheCardiovascular Research Institute, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; Diabetes, Obesity and Metabolism Institute, Department of Medicine, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; Graduate School of Biomedical Sciences, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. Electronic address: djamel.lebeche@mssm.edu.
Icahn School of Medicine at Mount Sinai · US

Funding

TRAINING PROGRAM IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007824 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GELB, BRUCE D · 1995 to 2022
$8.6M
NHLBI NIH HHS T32 HL007824
6 · The paper itself

Abstract

Cardiac fibrosis is characterized by excessive deposition of extracellular matrix proteins and myofibroblast differentiation. Our previous findings have implicated resistin in cardiac fibrosis; however, the molecular mechanisms underlying this process are still unclear. Here we investigated the role of resistin in fibroblast-to-myofibroblast differentiation and elucidated the pathways involved in this process. Fibroblast-to-myofibroblast transdifferentiation was induced with resistin or TGFβ1 in NIH-3T3 and adult cardiac fibroblasts. mRNA and protein expression of fibrotic markers were analyzed by qPCR and immunoblotting. Resistin-knockout mice, challenged with a high-fat diet (HFD) for 20 weeks to stimulate cardiac impairment, were analyzed for cardiac function and fibrosis using histologic and molecular methods. Cardiac fibroblasts stimulated with resistin displayed increased fibroblast-to-myofibroblast conversion, with increased levels of αSma, col1a1, Fn, Ccn2 and Mmp9, with remarkable differences in the actin network appearance. Mechanistically, resistin promotes fibroblast-to-myofibroblast transdifferentiation and fibrogenesis via JAK2/STAT3 and JNK/c-Jun signaling pathways, independent of TGFβ1. Resistin-null mice challenged with HFD showed an improvement in cardiac function and a decrease in tissue fibrosis and reduced mRNA levels of fibrogenic markers. These findings are the first to delineate the role of resistin in the process of cardiac fibroblast-to-myofibroblast differentiation via JAK/STAT3 and JNK/c-Jun pathways, potentially leading to stimulation of cardiac fibrosis.

Indexed as

AnimalsCell TransdifferentiationFemaleFibroblastsHEK293 CellsHumansJanus KinasesJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacNIH 3T3 CellsResistinJanus KinasesJNK Mitogen-Activated Protein KinasesResistinRetn protein, mouseStat3 protein, mouseSTAT3 Transcription FactorFibroblast/myofibroblast differentiationJAK2/STAT3JNK/c-JunMyocardial fibrosisResistinSP600125: JNK inhibitorWP1066: JAK2 inhibitor

Identifiers

PMID33524540
PMCPMC8085100
OpenAlexW3129183670

What OpenQuestion holds

Textmetadata
LicenceTDM
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.