ReviewJournal of inflammation research2026
Neutrophil Extracellular Traps in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Targets.
Review in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a clinical syndrome characterized by myocardial remodeling, pathological fibrosis, and chronic sterile inflammation. Within the pathophysiological network of HF and its complex comorbidities, neutrophil extracellular traps (NETs) have been identified as key pathological mediators driving tissue damage. This review aims to explore the regulatory mechanisms of NETs in the progression of heart failure (HF) and their cross-organ pathological effects, and to summarize the latest research advances in NET-targeted interventions for the treatment of HF. NETs are reticular structures composed of antimicrobial proteins, such as myeloperoxidase (MPO) and histones, attached to a decondensed DNA scaffold. Under pathological conditions, excessive NET release and impaired clearance trigger inflammatory cascades. Aberrant NETs formation significantly promotes cardiac remodeling and pathological fibrosis by mediating immunothrombosis, inducing cardiomyocyte apoptosis, and activating fibroblasts.NETs serve as a critical pathophysiological link connecting HF to systemic comorbidities. Therapeutic strategies targeting NETs primarily include inhibiting PAD4 or associated signaling axes to block NETs formation, utilizing enzymatic reactions to facilitate NETs clearance, uncovering the novel potential of established clinical agents, and employing nanotechnology-based precision delivery systems. These findings offer new avenues for precision immunotherapy in HF and highlight considerable potential for clinical translation.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.