Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure

Table 1

Molecular pathways of ventricular remodelling. Many mediators have either an adaptive role (in bold) at low doses or a maladaptive role, with chronic/intense stimulation.

	Molecular pathways activated by interaction with receptor	Effects on cardiomyocytes
Soluble mediator
Angiotensin II [28]	JNK; ERK	Apoptosis; Cell survival and growth
ROS [28, 60]	Cell damage; JAK/STAT	Apoptosis; Cell survival and growth
TNF- [28, 61, 62]	NF-κB; NF-κB	Apoptosis; Cell survival and growth
Growth factors (IGF-1, PDGF, GDF-15, HGF, and NRG-1) [28, 59, 63, 64]	PI3K/AKT; RAS/RAF/MEK/ERK	Cell survival and growth
Cardiotrophin-1 [28, 65]	JAK/STAT	Cell survival and growth
Cytosolic calcium [59, 66, 67]	Calpains (calcium-activated proteases); Calcineurin/NFAT	Apoptosis; Cell survival and growth
Catecholamines [68, 69]; (-adrenergic signalling)	PKA; ERK	Apoptosis; Cell survival and growth
Mechanical sensing of myocardial stretch
Integrins [54]	FAK	Cell survival and growth

JNK: Jun N-terminal kinase; ERK: extracellular-regulated kinase; JAK/STAT: Janus kinase/signal transducers and activators of transcription; ROS: reactive oxygen species; TNF-: tumor necrosis factor-; TRADD: TNF receptor-associated death domain; NF-κB: nuclear factor-κB; IGF-1: insulin-like growth factor-1; PDGF: platelet-derived growth factor; GDF-15: growth differentiation factor-15; HGF: hepatocyte growth factor; NRG-1: neuregulin-1; PI3K/AKT: phosphatidylinositol 3-kinase/AKT; NFAT: nuclear factor of activated T cells; PKA: protein kinase A; FAK: focal adhesion kinase.