Evidence map›Paper›PMID 38456501›Full record

ArticleJCI insight2024

Macrophage-enriched Sectm1a promotes efficient efferocytosis to attenuate ischemia/reperfusion-induced cardiac injury.

Xiaohong Wang, Wa Du, Yutian Li, Hui-Hui Yang, Yu Zhang, Rubab Akbar, Hannah Morgan, Tianqing Peng, Jing Chen, Sakthivel Sadayappan and 4 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Review
  4. Macrophage Efferocytosis in Heart.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Optimizing Neutrophil Recruitment to Tackle Bacterial Infections.American journal of respiratory cell and molecular biology · 2025
    Article
  13. Article
  14. Review
  15. Review
  16. Article
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

14 authors at 3 institutions in 2 countries.

Xiaohong WangDepartment of Pharmacology and Systems Physiology.
Wa DuDepartment of Cancer Biology, and.
Yutian LiDepartment of Pharmacology and Systems Physiology.
Hui-Hui YangDepartment of Pharmacology and Systems Physiology.
Yu ZhangDepartment of Pharmacology and Systems Physiology.
Rubab AkbarDepartment of Pharmacology and Systems Physiology.
Hannah MorganDivision of Cardiovascular Health and Disease, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Tianqing PengCentre for Critical Illness Research, Lawson Health Research Institute, London, Ontario, Canada.
Jing ChenDivision of Biomedical Informatics and.
Sakthivel SadayappanDivision of Cardiovascular Health and Disease, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Yueh-Chiang HuTransgenic Animal and Genome Editing Facility, Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Yanbo FanDepartment of Cancer Biology, and.
Wei HuangDivision of Cardiovascular Health and Disease, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Guo-Chang FanDepartment of Pharmacology and Systems Physiology.
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USLawson Health Research Institute · CA

Funding

Fast myosin binding protein-C and cardiac contractility in heart failureR01HL105826 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2011 to 2025
$4.5M
Lcn10 in Sepsis-Induced Vascular Leakage and Heart FailureR01HL160811 · NHLBI · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2022 to 2025
$2.7M
CCDC92 and Cardiovascular DiseaseR01HL167024 · NHLBI · UNIVERSITY OF CINCINNATI · PI Yanbo Fan · 2023 to 2026
$2.5M
The role of TFEB in aortic aneurysmsR01HL145176 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FAN, YANBO · 2019 to 2022
$2.2M
Alleviation of chemotherapy-induced cardiovascular toxicityR01HL171495 · NHLBI · UNIVERSITY OF CINCINNATI · PI Wa Du, Yanbo Fan · 2024 to 2026
$2.1M
Slow myosin binding protein-C in skeletal muscle physiologyR01AR078001 · NIAMS · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2020 to 2023
$1.8M
Mitochondrial R-loop in sepsis-induced cardiomyopathyR01HL163148 · NHLBI · UNIVERSITY OF CINCINNATI · PI Wei Huang · 2023 to 2026
$1.8M
Novel regulators of macrophage function to repair sterile inflammation-induced heart injuryR35GM149538 · NIGMS · UNIVERSITY OF CINCINNATI · PI Guo-Chang Fan · 2023 to 2026
$1.8M
IGF-2R is a new therapeutic target for cardiac ischemia-reperfusion injuryR01HL143490 · NHLBI · UNIVERSITY OF CINCINNATI · PI WANG, YIGANG · 2019 to 2022
$1.6M
Stimulating Access to Research in the University of Cincinnati Internal Medicine Residency ProgramR38HL155775 · NHLBI · UNIVERSITY OF CINCINNATI · PI Jack Rubinstein · 2021 to 2026
$1.6M
A novel strategy for heart failure therapeuticsR01HL168464 · NHLBI · UNIVERSITY OF CINCINNATI · PI Wei Huang, Yigang Wang · 2024 to 2026
$1.6M
Molecular mechanism of hypertrophic cardiomyopathy in populations of South Asian descendantsR01HL130356 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL105826NHLBI NIH HHS R01 HL130356NHLBI NIH HHS R01 HL143490NHLBI NIH HHS R01 HL145176NHLBI NIH HHS R01 HL160811NHLBI NIH HHS R01 HL163148NHLBI NIH HHS R01 HL167024NHLBI NIH HHS R01 HL168464NHLBI NIH HHS R38 HL155775NIAMS NIH HHS R01 AR078001NIGMS NIH HHS R01 GM132149NIGMS NIH HHS R35 GM149538
6 · The paper itself

Abstract

Efficient clearance and degradation of apoptotic cardiomyocytes by macrophages (collectively termed efferocytosis) is critical for inflammation resolution and restoration of cardiac function after myocardial ischemia/reperfusion (I/R). Here, we define secreted and transmembrane protein 1a (Sectm1a), a cardiac macrophage-enriched gene, as a modulator of macrophage efferocytosis in I/R-injured hearts. Upon myocardial I/R, Sectm1a-KO mice exhibited impaired macrophage efferocytosis, leading to massive accumulation of apoptotic cardiomyocytes, cardiac inflammation, fibrosis, and consequently, exaggerated cardiac dysfunction. By contrast, therapeutic administration of recombinant SECTM1A protein significantly enhanced macrophage efferocytosis and improved cardiac function. Mechanistically, SECTM1A could elicit autocrine effects on the activation of glucocorticoid-induced TNF receptor (GITR) at the surface of macrophages, leading to the upregulation of liver X receptor α (LXRα) and its downstream efferocytosis-related genes and lysosomal enzyme genes. Our study suggests that Sectm1a-mediated activation of the Gitr/LXRα axis could be a promising approach to enhance macrophage efferocytosis for the treatment of myocardial I/R injury.

Indexed as

Myocardial Reperfusion InjuryPhagocytosisAnimalsApoptosisEfferocytosisInflammationMacrophagesMembrane ProteinsMiceReperfusionMembrane ProteinsSECTM1A protein, mouseCardiologyCardiovascular diseaseCellular immune responseImmunologyMacrophages

Identifiers

PMID38456501
PMCPMC10972593
OpenAlexW4393034472

What Socratic holds

Textmetadata
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 Socratic graph.