Evidence map›Paper›PMID 39717608›Full record

ReviewHeliyon2024

Investigating the NF-κB signaling pathway in heart failure: Exploring potential therapeutic approaches.

Mohsen Ghiasi

Abstract readReview
In one paragraph

Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Trial
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  13. Immune modulatory potential ofToxicology research · 2025
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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

1 author.

Mohsen GhiasiRajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) syndrome is of great interest as an emerging epidemic. Due to the increasing elderly population worldwide, the total number of HF patients is increasing every day. This disease places a significant economic burden on the healthcare and treatment systems of developing societies, and this situation is very concerning. Despite many advances in the diagnosis and treatment of cardiovascular diseases, HF is still the main cause of death worldwide. This clinical syndrome has many cellular and molecular complications, which are often aggravated by increased levels of pro-inflammatory cytokines, which lead to adverse clinical outcomes. Nuclear factor kappa B (NF-κB), a pivotal family of transcription factors, plays a crucial role in various biological processes, particularly in inflammation, immune response, cell proliferation, and cell survival. Studies show that the NF-κB signaling pathway plays a role in modulating cardiac regeneration, apoptosis, and myocardial fibrosis. It has been found that the NF-κB signaling pathway can affect heart function and HF through the regulation of matrix metalloproteinases and fibrotic mediators. Also, the NF-κB pathway regulates cell activities in cardiac cardiomyocytes and regulates the function of this organ by establishing a precise interaction between apoptosis and pyroptosis. However, the exact molecular mechanisms of this influence have not been well defined and there are many scientific gaps in this matter. This review tries to highlights potential therapeutic strategies to target NF-κB, including the use of anti-inflammatory agents and genetic modulation, which may provide new ways to reduce cardiac fibrosis and improve outcomes in HF patients. Certainly, increasing understanding of the multifaceted role of NF-κB in HF can lead to innovative treatments aimed at reducing the growing number of patients worldwide.

Indexed as

Cell signalingHeart failureInflammationNF-κB pathway

Identifiers

PMID39717608
PMCPMC11664283

What Socratic 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 Socratic graph.