Table 1.
Biomarker
|
Pathophysiological pathway
|
Supporting evidence
|
LncRNA (LIPCAR, MIAT, SENCR) | Epigenetic regulation of multiple genes involved in diabetes and cardiac dysfunction | Liu et al[171]; Yan et al[172]; Carter et al[173]; de Gonzalo-Calvo et al[174] |
sST-2 | IL-33 decoy receptor that tones down Th2 inflammatory response via the IL-33/ST2/sST2 axis | Fousteris et al[164]; Kiencke et al[165] |
TGF-β | The main pro-fibrotic factor in heart failure: it modulates the fibroblast phenotype and function and mediates induction of EndoMT | Shaver et al[102]; Iglesias-De La Cruz et al[104]; Asbun et al[105] |
Galectin-3 | Mediator by which multiple molecules (e.g. angiotensin II and aldosterone) exert their pro-fibrotic activity and promote oxidative stress | Ho et al[146]; Ueland et al[147]; Sharma et al[148] |
GDF-15 | Regulator of inflammatory pathways involved in regulation of apoptosis, cell repair and cell growth | Berezin[123]; Dominguez-Rodriguez et al[130] |
RNA: Ribonucleic acid; LncRNA: Long noncoding ribonucleic acid; LIPCAR: Long intergenic non-coding ribonucleic acid predicting cardiac remodeling; MIAT: Myocardial infarction-associated transcript; SENCR: Smooth muscle and endothelial cell-enriched migration/differentiation-associated long noncoding ribonucleic acid; sST2: Soluble form of suppression of tumorigenicity 2; GDF-15: Growth differentiation factor-15; TGF-β: Transforming growth factor-β; EndoMT: Endothelial-mesenchymal transition.