Evidence map›Paper›PMID 39142438›Full record

ReviewJournal of molecular and cellular cardiology2024

Mechanisms of the septic heart: From inflammatory response to myocardial edema.

Dihan Fan, Rongxue Wu

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Article
  2. Article
  3. Septic cardiomyopathy: Fact or fiction?American heart journal plus : cardiology research and practice · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Association Between Myocardial Dysfunction and Septic Shock.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

2 authors.

Dihan FanPsychiatric Genetics Group, McGill University, Canada.
Rongxue WuDepartment of Medicine, Section of Cariology, Biological Sciences Division, The University of Chicago, IL, United States. Electronic address: rwu3@uchicago.edu.

Funding

Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI RONALD N COHEN · 2013 to 2026
$20.9M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
ARNT: A novel regulator of cardiac vascular endothelial barrier function in heart failureR01HL140114 · NHLBI · UNIVERSITY OF CHICAGO · PI WU, RONGXUE · 2019 to 2023
$2.1M
NCATS NIH HHS UL1 TR000430NHLBI NIH HHS R01 HL140114NIDDK NIH HHS P30 DK020595
6 · The paper itself

Abstract

Sepsis-induced myocardial dysfunction (SIMD), also known as sepsis-induced cardiomyopathy (SICM), is linked to significantly increased mortality. Despite its clinical importance, effective therapies for SIMD remain elusive, largely due to an incomplete understanding of its pathogenesis. Over the past five decades, research involving both animal models and human studies has highlighted several pathogenic mechanisms of SICM, yet many aspects remain unexplored. Initially thought to be primarily driven by inflammatory cytokines, current research indicates that these alone are insufficient for the development of cardiac dysfunction. Recent studies have brought attention to additional mechanisms, including excessive nitric oxide production, mitochondrial dysfunction, and disturbances in calcium homeostasis, as contributing factors in SICM. Emerging clinical evidence has highlighted the significant role of myocardial edema in the pathogenesis of SICM, particularly its association with cardiac remodeling in septic shock patients. This review synthesizes our current understanding of SIMD/SICM, focusing on myocardial edema's contribution to cardiac dysfunction and the critical role of the bradykinin receptor B1 (B1R) in altering myocardial microvascular permeability, a potential key player in myocardial edema development during sepsis. Additionally, this review briefly summarizes existing therapeutic strategies and their challenges and explores future research directions. It emphasizes the need for a deeper understanding of SICM to develop more effective treatments.

Indexed as

CardiomyopathiesInflammationMyocardiumSepsisAnimalsEdemaEdema, CardiacHumansCardiac edemaEndothall barrier functionMolecular mechanismssepsisSepsis-induced cardiomyopathyTreatments

Identifiers

PMID39142438
PMCPMC13104036

What OpenQuestion holds

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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.