ReviewMolecular biology reports2025
Molecular mechanisms and complications of TNF blockade in heart failure: targeting signalling and genetic determinants of therapeutic response.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Pathogenic role of mitochondrial DNA mutations in heart failure: clinical features, mechanisms, and therapeutic prospects.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumour necrosis factor-alpha (TNF) plays a pivotal role in the inflammatory cascade associated with both cardiovascular pathology and autoimmune conditions. While anti-TNF therapies have shown clinical efficacy in immune-mediated disorders, their use in patients with chronic heart failure (CHF) has produced inconsistent adverse outcomes. This review explores the molecular and cellular mechanisms underlying the inconsistent effects of TNF blockade in heart failure, with a particular focus on receptor-specific signalling, cytokine gene regulation, and intracellular consequences of TNF antagonism. This article highlights the divergent roles of tumor necrosis factor receptor 1 and 2 (TNFR1; TNFR2) in cardiac tissue, highlighting how non-selective TNF neutralisation disrupts the balance between apoptotic and regenerative pathways. Key signalling cascades such as NF-κB, p38 MAPK, and PI3K/Akt are discussed in the context of anti-TNF therapy and its effects on myocardial survival, remodelling, and vascular integrity. The review also addresses genetic polymorphisms (e.g. TNF - 308G > A) that may influence therapeutic response and susceptibility to adverse effects. Large-scale clinical trials are needed to assess the long-term safety and effectiveness of receptor-selective TNF modulation. By integrating personalized medicine nanomedicine, biotechnology, and next-generation TNF-targeting strategies could help overcome previous therapeutic failures and lead to more effective treatments for heart disease patients. A deeper understanding of TNF signalling at the molecular level suggests that future therapeutic strategies should prioritise receptor-selective modulation and patient stratification based on genetic and inflammatory biomarkers. Such precision approaches may help overcome the limitations of broad TNF inhibition and enable safer, targeted interventions in CHF.
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Registered trials
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.