Evidence map›Paper›PMID 35664861›Full record

ArticleCurrent opinion in physiology2021

Neutrophil crosstalk during cardiac wound healing after myocardial infarction.

Upendra Chalise, Mediha Becirovic-Agic, Merry L Lindsey

Open access · hybridAbstract read
In one paragraph

Article in Current opinion in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  5. Review
  6. Article
  7. Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025
    Review
  8. Role of Trained Immunity in Heath and Disease.Current cardiology reports · 2025
    Review
  9. Review
  10. Article
  11. Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
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.

Upendra ChaliseDepartment of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, NE 68198; and Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68105.
Mediha Becirovic-AgicDepartment of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, NE 68198; and Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68105.
Merry L LindseyDepartment of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, NE 68198; and Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68105.
Nebraska Medical Center · US

Funding

Tracking and Evaluation CoreU54GM115458 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GUDA, CHITTIBABU · 2016 to 2025
$42.8M
MMP-12 as an Endogenous Post-MI Resolution Promoting FactorR01HL137319 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LINDSEY, MERRY L. · 2019 to 2022
$1.5M
BLRD VA I01 BX000505NHLBI NIH HHS R01 HL137319NIGMS NIH HHS U54 GM115458
6 · The paper itself

Abstract

Myocardial infarction (MI) initiates an intense inflammatory response that induces neutrophil infiltration into the infarct region. Neutrophils commence the pro-inflammatory response that includes upregulation of cytokines and chemokines (e.g., interleukin-1 beta) and degranulation of pre-formed proteases (e.g., matrix metalloproteinases -8 and -9) that degrade existing extracellular matrix to clear necrotic tissue. An increase or complete depletion of neutrophils both paradoxically impair MI resolution, indicating a complex role of neutrophils in cardiac wound healing. Following pro-inflammation, the neutrophil shifts to a reparative phenotype that promotes inflammation resolution and aids in scar formation. Across the shifts in phenotype, the neutrophil communicates with other cells to coordinate repair and scar formation. This review summarizes our current understanding of neutrophil crosstalk with cardiomyocytes and macrophages during MI wound healing.

Indexed as

cardiac wound healingcardiomyocyteinflammationleukocytemacrophage

Identifiers

PMID35664861
PMCPMC9159545
OpenAlexW4210501947

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.