Table 1.
Mechanisms of alcohol-induced heart damage.
| Mechanisms | Effectors |
|---|---|
| Interference with cell signaling and calcium transients [16,17] | MAPK, TGF-β, PKC, PPARγ, MMPs, NF-κβ, PAI-1 |
| Decrease in excitation-contraction coupling mechanisms [17,18,19] | intracellular [Ca]2+ transients, L-type Ca2+ channel |
| Induction of oxidative damage [20,21] | ROS, SOD, acetaldehyde |
| Pro-inflammatory effect [22] | IL-2, TNF-α, NF-κβ |
| Induction of apoptosis [23,24] | FAS, TNF-α, TGF-β, Bax-Bcl-2, caspases 3,6 |
| Induction of fibrosis [25] | TLR-4, TGF-β |
| Protein-adduct formation [26] | protein-ethanol-adducts |
| malondialdehyde-DNA adducts | |
| Disruption in protein synthesis [27] | decrease in ribosomal protein synthesis, actin, myosin, troponin, titin |
| Increased glycogen deposition [28,29] | glycogen synthase kinase-3β, PARP |
| Renin-angiotensin-aldosterone activation [30] | renin, angiotensin, aldosterone, p38 MAPK/Smad |
| Interference in hormone-growth factors [31,32] | myostatin, ghrelin, leptin, IGF-1 |
| Interference in regulatory cardiomyokines [33,34] | FGF21 |
| Decrease in myocyte regeneration [35] | myostatin, IGF-1 |
| Impairment of extracellular matrix turnover [16] | cytoskeletal structure, connexin channel, desmosome contacts |
| Imbalance between cardiac lesions/repair mechanisms [9] | cell apoptosis and necrosis increased myocardial fibrosis decreased myocyte regeneration |