Evidence map›Paper›PMID 36740099›Full record

ReviewImmunology letters2023

Cellular mechanisms underlying the impairment of macrophage efferocytosis.

Yonggang Ma, Scott S Kemp, Xiaoyuan Yang, Mack H Wu, Sarah Y Yuan

Open access · greenAbstract readReview
In one paragraph

Review in Immunology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Mitochondrial checkpoint for interferon responses in macrophages.Exploration of targeted anti-tumor therapy · 2026
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. GATA2 Mediates Macrophage Proliferation During Atherosclerosis.Journal of the American Heart Association · 2025
    Article
  13. Review
  14. Review
  15. 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

5 authors at 1 institution in 1 country.

Yonggang MaDepartment of Molecular Pharmacology and Physiology, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA.
Scott S KempDepartment of Molecular Pharmacology and Physiology, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA.
Xiaoyuan YangDepartment of Molecular Pharmacology and Physiology, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA.
Mack H WuDepartment of Surgery, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA.
Sarah Y YuanDepartment of Molecular Pharmacology and Physiology, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA; Department of Surgery, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA. Electronic address: syuan@usf.edu.
University of South Florida · US

Funding

Vascular Barrier Leakage in InflammationR35HL150732 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI Sarah Y Yuan · 2020 to 2026
$6.2M
T Lymphopenia in Ischemic Heart FailureR01HL164446 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI Yonggang Ma · 2022 to 2026
$2.0M
Endothelial glycocalyx shedding in septic injuryR01GM142110 · NIGMS · UNIVERSITY OF SOUTH FLORIDA · PI WU, MACK H, YUAN, SARAH Y · 2022 to 2025
$1.9M
Extracellular Histones in Burn-induced Microvascular HyperpermeabilityR01GM143138 · NIGMS · UNIVERSITY OF SOUTH FLORIDA · PI WU, MACK H · 2022 to 2025
$1.3M
Training in Research on Vascular Inflammation and InjuryT32HL160529 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI Sarah Y Yuan · 2022 to 2026
$1.1M
Molecular Control of Gut Permeability in TraumaI01BX000799 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI WU, MACK H · 2011 to 2023
–
BLRD Research Career Scientist Award ApplicationIK6BX004210 · VA · JAMES A. HALEY VA MEDICAL CENTER · PI WU, MACK H · 2018 to 2025
–
BLRD VA I01 BX000799BLRD VA IK6 BX004210NHLBI NIH HHS R01 HL164446NHLBI NIH HHS R35 HL150732NHLBI NIH HHS T32 HL160529NIGMS NIH HHS R01 GM142110NIGMS NIH HHS R01 GM143138
6 · The paper itself

Abstract

The phagocytosis and clearance of dying cells by macrophages, a process termed efferocytosis, is essential for both maintaining homeostasis and promoting tissue repair after infection or sterile injury. If not removed in a timely manner, uncleared cells can undergo secondary necrosis, and necrotic cells lose membrane integrity, release toxic intracellular components, and potentially induce inflammation or autoimmune diseases. Efferocytosis also initiates the repair process by producing a wide range of pro-reparative factors. Accumulating evidence has revealed that macrophage efferocytosis defects are involved in the development and progression of a variety of inflammatory and autoimmune diseases. The underlying mechanisms of efferocytosis impairment are complex, disease-dependent, and incompletely understood. In this review, we will first summarize the current knowledge about the normal signaling and metabolic processes of macrophage efferocytosis and its importance in maintaining tissue homeostasis and repair. We then will focus on analyzing the molecular and cellular mechanisms underlying efferocytotic abnormality (impairment) in disease or injury conditions. Next, we will discuss the potential molecular targets for enhanced efferocytosis in animal models of disease. To provide a balanced view, we will also discuss some deleterious effects of efferocytosis.

Indexed as

ApoptosisPhagocytosisAnimalsInflammationMacrophagesSignal TransductionApoptosisEfferocytosisInflammation resolutionMacrophageNeutrophilPhagocytosis

Identifiers

PMID36740099
PMCPMC9992097
OpenAlexW4319071941

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.