ArticleCureus2025
401-Gene Signature of Myocardial Dysfunction in Human Heart Failure: A Transcriptomic Analysis.
Article in Cureus, 2025. 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Heart failure is a complex clinical syndrome characterized by the molecular remodeling of myocardial tissue that significantly impacts global health outcomes. Transcriptomic analysis offers powerful tools to identify disease-specific gene expression signatures and potential therapeutic targets. Methods We analyzed publicly available gene expression data from the Gene Expression Omnibus (GEO) dataset GSE57345, comprising 313 left ventricular tissue samples (295 controls, 18 heart failure) profiled using Affymetrix Human Gene 1.1 ST Arrays (Thermo Fisher Scientific, Waltham, Massachusetts, United States). Differential expression analysis was performed using limma with Benjamini-Hochberg multiple testing correction. Results We identified 401 significantly differentially expressed genes (adjusted p<0.05) between heart failure and control samples. The molecular signature showed balanced dysregulation with 198 genes upregulated and 203 genes downregulated in heart failure. Pathway analysis revealed significant enrichment in mitochondrial dysfunction, immune activation, and extracellular matrix remodeling pathways. Top dysregulated genes included AIDC1, SECA1, PVRL2, PLD1, and KTR3CL3, with high statistical significance (p<1×10⁻⁶) despite modest fold changes characteristic of complex disease pathophysiology. Cross-validation with established heart failure signatures showed significant overlap (31.7% concordance), confirming biological relevance. Conclusions This 401-gene transcriptomic signature provides insights into heart failure molecular mechanisms and represents a potential resource for biomarker development and therapeutic target identification. The balanced pattern of gene dysregulation reflects the comprehensive transcriptional remodeling underlying cardiac dysfunction and supports precision medicine approaches for heart failure diagnosis and treatment stratification.
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.