Evidence map›Paper›PMID 32902739›Full record

ReviewCardiovascular drugs and therapy2020

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure.

Anis Hanna, Nikolaos G Frangogiannis

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular drugs and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 264 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
264citing papers in PubMed, 4 pooled it
28.8field-weighted citation impact, top 1% 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

264 citing papers in PubMed, 4 syntheses or guidelines pooled it, 394 citations in OpenAlex.

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  16. A novel mouse model of adenine-supplemented high-fat diet induced cardiovascular-kidney-metabolic syndrome.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  17. Review
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  19. Cardiac Modulation byCurrent issues in molecular biology · 2026
    Article
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204 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Anis HannaDepartment of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, 1300 Morris Park Avenue Forchheimer G46B, Bronx, NY, 10461, USA.
Nikolaos G FrangogiannisDepartment of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, 1300 Morris Park Avenue Forchheimer G46B, Bronx, NY, 10461, USA. nikolaos.frangogiannis@einstein.yu.edu.ORCID 0000-0002-8186-5131
Albert Einstein College of Medicine · US

Funding

Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
Regulation of the TGF-beta superfamily in the remodeling and failing heartR01HL149407 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2020 to 2023
$2.2M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NHLBI NIH HHS R01 HL149407
6 · The paper itself

Abstract

Heart failure exhibits remarkable pathophysiologic heterogeneity. A large body of evidence suggests that regardless of the underlying etiology, heart failure is associated with induction of cytokines and chemokines that may contribute to the pathogenesis of adverse remodeling, and systolic and diastolic dysfunction. The pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 have been extensively implicated in the pathogenesis of heart failure. Inflammatory cytokines modulate phenotype and function of all myocardial cells, suppressing contractile function in cardiomyocytes, inducing inflammatory activation in macrophages, stimulating microvascular inflammation and dysfunction, and promoting a matrix-degrading phenotype in fibroblasts. Moreover, cytokine-induced growth factor synthesis may exert chronic fibrogenic actions contributing to the pathogenesis of heart failure with preserved ejection fraction (HFpEF). In addition to their role in adverse cardiac remodeling, some inflammatory cytokines may also exert protective actions on cardiomyocytes under conditions of stress. Chemokines, such as CCL2, are also upregulated in failing hearts and may stimulate recruitment of pro-inflammatory leukocytes, promoting myocardial injury, fibrotic remodeling, and dysfunction. Although experimental evidence suggests that cytokine and chemokine targeting may hold therapeutic promise in heart failure, clinical translation remains challenging. This review manuscript summarizes our knowledge on the role of TNF-α, IL-1, IL-6, and CCL2 in the pathogenesis of heart failure, and discusses the promises and challenges of targeted anti-cytokine therapy. Dissection of protective and maladaptive cellular actions of cytokines in the failing heart, and identification of patient subsets with overactive or dysregulated myocardial inflammatory responses are required for design of successful therapeutic approaches.

Indexed as

AnimalsAnti-Inflammatory AgentsChemokinesCytokinesHeart FailureHumansMolecular Targeted TherapyMyocytes, CardiacSignal TransductionTranslational Research, BiomedicalVentricular Function, LeftVentricular RemodelingAnti-Inflammatory AgentsChemokinesCytokinesChemokineCytokineHeart failureInflammationInterleukin-1TNF-α

Identifiers

PMID32902739
PMCPMC7479403
OpenAlexW3086485795

What OpenQuestion holds

Textmetadata
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.