Evidence map›Paper›PMID 32673537›Full record

ReviewCirculation research2020

Myofibroblasts and Fibrosis: Mitochondrial and Metabolic Control of Cellular Differentiation.

Andrew A Gibb, Michael P Lazaropoulos, John W Elrod

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 papers.

0numbers the graph read from it
0cells of the map it votes in
272citing papers in PubMed
26.5field-weighted citation impact, top 1% 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

272 citing papers in PubMed, 396 citations in OpenAlex.

  1. Review
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  8. Therapeutic Lithium Enhances Klotho Expression and Mitochondrial Size and Branching in Human Cardiac Fibroblasts Involving Nuclear Factor-kappa B Inhibition.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Article
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  12. Next-generation molecular imaging of cardiac fibrosis.The international journal of cardiovascular imaging · 2026
    Review
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212 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Andrew A GibbFrom the Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Michael P LazaropoulosFrom the Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
John W ElrodFrom the Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Temple University · US

Funding

Small and large animal surgery, physiology and histologyP01HL134608 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI Raj Kishore · 2017 to 2026
$21.0M
Targeting Pathways Involved in Cardiac Injury for Novel Repair StrategiesP01HL147841 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KOCH, WALTER J. · 2020 to 2024
$11.4M
Molecular composition of the mitochondrial calcium uniporter and cardiac pathophysiologyR01HL142271 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI ELROD, JOHN WILLIAM, HAJNOCZKY, GYORGY · 2018 to 2021
$3.0M
Mechanisms of mitochondrial calcium exchange in heart failureR01HL123966 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI ELROD, JOHN WILLIAM · 2014 to 2018
$2.3M
Novel Molecular Mechanisms of Programmed NecrosisR01HL136954 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI ELROD, JOHN WILLIAM · 2017 to 2020
$1.6M
The Role of Acetyl-CoA Metabolism in Epigenetic Regulation of Myofibroblast DifferentiationF30HL152564 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI LAZAROPOULOS, MICHAEL · 2020 to 2024
$204k
Metabolic control of cellular differentiation and the fibrotic responseF32HL145914 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI GIBB, ANDREW A · 2019 to 2021
$194k
NHLBI NIH HHS F30 HL152564NHLBI NIH HHS F32 HL145914NHLBI NIH HHS P01 HL134608NHLBI NIH HHS P01 HL147841NHLBI NIH HHS R01 HL123966NHLBI NIH HHS R01 HL136954NHLBI NIH HHS R01 HL142271
6 · The paper itself

Abstract

Cardiac fibrosis is mediated by the activation of resident cardiac fibroblasts, which differentiate into myofibroblasts in response to injury or stress. Although myofibroblast formation is a physiological response to acute injury, such as myocardial infarction, myofibroblast persistence, as occurs in heart failure, contributes to maladaptive remodeling and progressive functional decline. Although traditional pathways of activation, such as TGFβ (transforming growth factor β) and AngII (angiotensin II), have been well characterized, less understood are the alterations in mitochondrial function and cellular metabolism that are necessary to initiate and sustain myofibroblast formation and function. In this review, we highlight recent reports detailing the mitochondrial and metabolic mechanisms that contribute to myofibroblast differentiation, persistence, and function with the hope of identifying novel therapeutic targets to treat, and potentially reverse, tissue organ fibrosis.

Indexed as

Cell DifferentiationEnergy MetabolismAnimalsCalcium SignalingFibrosisHeart DiseasesHumansMitochondria, HeartMyofibroblastsfibrosisheart failuremetabolismmitochondriamyofibroblast

Identifiers

PMID32673537
PMCPMC7982967
OpenAlexW3043390187

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.