Evidence map›Paper›PMID 31434807›Full record

ArticleJCI insight2019

Antiinflammatory activity of ANGPTL4 facilitates macrophage polarization to induce cardiac repair.

Dong Im Cho, Hye-Jin Kang, Ju Hee Jeon, Gwang Hyeon Eom, Hyang Hee Cho, Mi Ra Kim, Meeyoung Cho, Hye-Yun Jeong, Hyen Chung Cho, Moon Hwa Hong and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Review
  3. The PPARβ/Delta-Induced Mesenchymal Stromal Cell Secretome Has Cytoprotective Effects via ANGPTL4 in a Pre-Clinical Model of Acute Lung Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  7. Article
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  18. Article
  19. Genetic Insights Into Coronary Microvascular Disease.Microcirculation (New York, N.Y. : 1994) · 2025
    Review
  20. Article

3 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

12 authors at 2 institutions in 1 country.

Dong Im ChoCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Hye-Jin KangCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Ju Hee JeonCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Gwang Hyeon EomDepartment of Pharmacology, Chonnam National University Medical School, Gwangju, Korea.
Hyang Hee ChoCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Mi Ra KimCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Meeyoung ChoCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Hye-Yun JeongCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Hyen Chung ChoCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Moon Hwa HongCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Yong Sook KimCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Youngkeun AhnCell Regeneration Research Center, Chonnam National University Hospital, Gwangju, Korea.
Chonnam National University Hospital · KRChonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) can suppress pathological inflammation. However, the mechanisms underlying the association between MSCs and inflammation remain unclear. Under coculture conditions with macrophages, MSCs highly expressed angiopoietin-like 4 (ANGPTL4) to blunt the polarization of macrophages toward the proinflammatory phenotype. ANGPTL4-deficient MSCs failed to inhibit the inflammatory macrophage phenotype. In inflammation-related animal models, the injection of coculture medium or ANGPTL4 protein increased the antiinflammatory macrophages in both peritonitis and myocardial infarction. In particular, cardiac function and pathology were markedly improved by ANGPTL4 treatment. We found that retinoic acid-related orphan receptor α (RORα) was increased by inflammatory mediators, such as IL-1β, and bound to ANGPTL4 promoter in MSCs. Collectively, RORα-mediated ANGPTL4 induction was shown to contribute to the antiinflammatory activity of MSCs against macrophages under pathological conditions. This study suggests that the capability of ANGPTL4 to induce tissue repair is a promising opportunity for safe stem cell-free regeneration therapy from a translational perspective.

Indexed as

Macrophage ActivationAngiopoietin-Like Protein 4AnimalsAnti-Inflammatory Agents, Non-SteroidalCell PolarityCells, CulturedCoculture TechniquesDisease Models, AnimalHumansInflammationInflammation MediatorsMacrophagesMaleMesenchymal Stem CellsMiceMice, Inbred BALB CAngiopoietin-Like Protein 4Anti-Inflammatory Agents, Non-SteroidalInflammation MediatorsNuclear Receptor Subfamily 1, Group F, Member 1Receptors, Retinoic AcidRORA protein, humanCardiologyCardiovascular diseaseCytokinesInflammationMacrophages

Identifiers

PMID31434807
PMCPMC6777833
OpenAlexW2969772586

What OpenQuestion holds

Textmetadata
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.