Evidence map›Paper›PMID 39938482›Full record

ArticleImmunity2025

Early-age efferocytosis directs macrophage arachidonic acid metabolism for tissue regeneration.

Connor Lantz, Amanda Becker, Matthew DeBerge, Mallory Filipp, Kristofor Glinton, Aparnaa Ananthakrishnan, Jessica Urbanczyk, Madeline Cetlin, Afnan Alzamroon, Ahmed Abdel-Latif and 3 more

Abstract read
In one paragraph

Article in Immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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. General View of Arachidonic Acid (AA) Metabolism.Reviews of physiology, biochemistry and pharmacology · 2027
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
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  9. Article
  10. Article
  11. Article
  12. Macrophage Efferocytosis in Heart.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  13. Suppression of cardiac allograft vasculopathy by a macrophage efferocytosis receptor.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
    Article
  14. Article
  15. Review
  16. Article
  17. Review
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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

13 authors.

Connor LantzDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA; Comprehensive Transplant Center, Northwestern University, Feinberg School of Medicine, Chicago, IL, 60611, USA. Electronic address: connor.lantz@northwestern.edu.
Amanda BeckerDepartment of Pediatrics, Feinberg School of Medicine, Chicago, IL 60611, USA.
Matthew DeBergeDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Mallory FilippDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Kristofor GlintonDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Aparnaa AnanthakrishnanDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Jessica UrbanczykDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Madeline CetlinDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Afnan AlzamroonUniversity of Michigan, Ann Arbor, MI 48109, USA.
Ahmed Abdel-LatifUniversity of Michigan, Ann Arbor, MI 48109, USA.
Matthew SpiteCenter for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Zhi-Dong GeDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA.
Edward B ThorpDepartment of Pathology, Feinberg School of Medicine, Chicago, IL 60611, USA; Department of Pediatrics, Feinberg School of Medicine, Chicago, IL 60611, USA; Heart Center, Stanley Manne Children's Research Institute, Ann & Robert Lurie Children's Hospital, Chicago, IL 60611, USA; Comprehensive Transplant Center, Northwestern University, Feinberg School of Medicine, Chicago, IL, 60611, USA. Electronic address: ebthorp@northwestern.edu.

Funding

CELLULAR &MOLECULAR BASIS OF DISEASE TRAINING PROGRAMT32GM008061 · NIGMS · NORTHWESTERN UNIVERSITY · PI CARTHEW, RICHARD W. · 1985 to 2022
$17.1M
Role of Inflammation-Resolving Lipid Mediators In Ischemic RevascularizationR01HL106173 · NHLBI · UNIVERSITY OF LOUISVILLE · PI SPITE, MATTHEW R · 2011 to 2023
$5.7M
Efferocytosis-Directed Inflammation Resolution and Repair in the Hypoxic HeartR01HL122309 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THORP, EDWARD BENJAMIN · 2014 to 2024
$5.0M
DHA-derived resolvin production andsignaling in tissue repair macrophages in metabolic diseaseR01DK124782 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI NAGY, LASZLO, SPITE, MATTHEW R · 2020 to 2023
$2.3M
Phagocyte Crosstalk in the Balance of Inflammation & Cardiac DiseaseR35HL177401 · NHLBI · NORTHWESTERN UNIVERSITY · PI Edward Benjamin Thorp · 2025 to 2026
$2.1M
Contributions of Myeloid Metabolism to Diastolic DysfunctionR01HL159964 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THORP, EDWARD BENJAMIN · 2022 to 2024
$1.5M
Elucidating the Mechanisms by which Macrophages and their TAM Receptors Promote Cardiac RegenerationF31HL158200 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LANTZ, CONNOR WILLIAM · 2022 to 2023
$85k
American Heart Association-American Stroke Association 829400American Heart Association-American Stroke Association AHA_829400NHLBI NIH HHS F31 HL158200NHLBI NIH HHS R01 HL106173NHLBI NIH HHS R01 HL122309NHLBI NIH HHS R01 HL159964NHLBI NIH HHS R35 HL177401NIDDK NIH HHS R01 DK124782NIGMS NIH HHS T32 GM008061
6 · The paper itself

Abstract

In response to organ injury in adults, macrophages often promote scarring, yet during early life, they are required for tissue regeneration. To elucidate the mechanisms underlying age-associated regeneration, we compared the macrophage injury response in newborn versus adult hearts. Single-cell analysis revealed an accumulation of tissue-resident macrophages in neonates that were selectively polarized for apoptotic cell recognition and uptake (efferocytosis). Ablation of the apoptotic cell recognition receptor Mertk in newborns prevented cardiac regeneration. These findings could be attributed to reprogramming of macrophage gene expression that was required for biosynthesis of the eicosanoid thromboxane A

Indexed as

Arachidonic AcidMacrophagesPhagocytosisRegenerationAnimalsAnimals, NewbornApoptosisCell Proliferationc-Mer Tyrosine KinaseEfferocytosisHeartMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacReceptors, Thromboxane A2, Prostaglandin H2Arachidonic Acidc-Mer Tyrosine KinaseMertk protein, mouseReceptors, Thromboxane A2, Prostaglandin H2agingarachidonic acidefferocytosisheartimmunometabolismmacrophageproliferationregenerationthromboxane

Identifiers

PMID39938482
PMCPMC11839170

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Registered trials

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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.