ReviewFrontiers in cardiovascular medicine2026
Pediatric dilated cardiomyopathy and the progression to heart failure: mechanisms and interventions focusing on the "gene-inflammation-metabolism" axis.
Review in Frontiers in cardiovascular medicine, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dilated cardiomyopathy (DCM) is the most common cardiomyopathy in children and a leading indication for heart transplantation. Despite considerable progress in understanding its genetic architecture, translating these insights into improved outcomes for children remains challenging. The pathophysiology of pediatric dilated cardiomyopathy is highly complex, extending beyond a simple monogenic model to encompass intricate interactions between genetic predisposition, inflammatory triggers, and metabolic dysregulation. This review systematically synthesizes current evidence on the mechanisms driving heart failure progression in pediatric dilated cardiomyopathy, focusing on the integrated framework of the "gene-inflammation-metabolism" axis. We begin by outlining the genetic landscape of pediatric dilated cardiomyopathy, highlighting key pathogenic genes and their associated phenotypes, with particular emphasis on features distinct from adult disease. We then explore how environmental "second hits" (such as viral infection and autoimmune responses) trigger excessive inflammatory reactions, and discuss the significance of special clinical phenomena such as "hot phase" myocarditis in genetically susceptible children. Concurrently, we systematically examine the metabolic reprogramming of the failing heart, including mitochondrial dysfunction, substrate utilization shifts, insulin resistance, and iron metabolism disturbances, analyzing how these processes further compromise energy-starved cardiomyocytes. By integrating these three interconnected domains, this review presents a pediatric-specific triaxial framework that unifies known DCM pathways into a single actionable model for precision risk stratification and targeted therapy. This framework supports the development of novel biomarkers, multi-dimensional risk stratification strategies, and targeted interventions-ranging from anti-inflammatory agents and metabolic modulators to gene therapy, psychological support, and AI-assisted risk prediction. This review aims to provide a novel theoretical framework and practical roadmap for the clinical management and future research of pediatric dilated cardiomyopathy.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.