Evidence map›Paper›PMID 24486305›Full record

ReviewLife sciences2014

Innate immunity and cardiomyocytes in ischemic heart disease.

Li Lin, Anne A Knowlton

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Life sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.5field-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

44 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  3. Review
  4. NF-Frontiers in cardiovascular medicine · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Innate and adaptive immunity in acute myocarditis.International journal of cardiology · 2024
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Can the calcium-regulating hormones counteract the detrimental impact of pro-inflammatory damage-associated molecular patterns in the development of heart failure?Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2021
    Review
  18. Review
  19. Article
  20. 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

2 authors at 2 institutions in 2 countries.

Li LinDepartment of Physiology, Second Military Medical University, Shanghai 200433, China.
Anne A KnowltonMolecular and Cellular Cardiology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA; Department of Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA; Department of Pharmacology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA; The Northern California VA, Sacramento, CA, USA. Electronic address: aaknowlton@ucdavis.edu.
Northern California Research · USSecond Military Medical University · CN

Funding

Human Cardiomyopathy and HSP60R01HL077281 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI KNOWLTON, ANNE A · 2004 to 2012
$3.1M
HSPs, Inflammatory Response and Cardiovascular DiseaseR01HL079071 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KNOWLTON, ANNE A · 2006 to 2014
$2.7M
NHLBI NIH HHS HL077281NHLBI NIH HHS HL079071NHLBI NIH HHS R01 HL077281NHLBI NIH HHS R01 HL079071
6 · The paper itself

Abstract

Myocardial ischemia/reperfusion (I/R) is the most common cause of myocardial inflammation, which is primarily a manifestation of the innate immune responses. Innate immunity is activated when pattern recognition receptors (PRRs) respond to molecular patterns common to microbes and to danger signals expressed by injured or infected cells, so called pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). The expression of various PRRs in cardiomyocytes and the release of DAMPs from cardiomyocytes subjected to I/R injury, through active mechanisms as well as passive processes, enable cardiomyocytes to generate innate immune responses. Studies in isolated heart and cardiomyocytes have confirmed the inflammatory and functional effects of cardiac PRRs especially Toll-like receptors in response to I/R-derived DAMPs, such as heat shock proteins. This review addresses the active role of cardiomyocytes in mediating innate inflammatory responses to myocardial I/R. We propose that cardiomyocytes act as innate immune cells in myocardial I/R injury.

Indexed as

Immunity, InnateAnimalsHeat-Shock ProteinsHMGB1 ProteinHumansLectins, C-TypeMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacNod Signaling Adaptor ProteinsToll-Like ReceptorsHeat-Shock ProteinsHMGB1 ProteinLectins, C-TypeNod Signaling Adaptor ProteinsToll-Like ReceptorsCardiomyocytesHeartInflammationInnate immunityIschemia/reperfusionNF-κBPattern recognition receptorTLR2TLR4

Identifiers

PMID24486305
PMCPMC3970925
OpenAlexW2075089814

What Socratic 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 Socratic graph.