|
| Extracellular signals | Receptor | Signal pathway | Biological effects | Clinical effects on HF patients |
| In vitro | In vivo |
|
| Triiodothyronine (T3) | TR1α (thyroid hormone receptor α1) | ① AMPK↑ [10]
② Regulating IGF1/IGF1-R/AKT [13]
③ ERK↑ [11] | CM growth↑ [10],
CM maturation↑ [4],
myofilament proteins expression↑ [12],
L-type Ca2+ channel↓ [6] | CM proliferation and cardiac regeneration↑ [2],
cardiac ischemia-reperfusion injury↓ [15–17],
cardiac remodeling↓ [16, 18, 19] | Ventricular performance↑ [23],
cardiac index↑ [24],
cardiac function not improved [25], |
|
| Neuregulin-1 (NRG1) | ErbB receptor | ① ERK1/2MAPK↑ [34]
② PI3KAKT↑ [35, 36]
③ FAK↑ [37] | CM survival↑ [36],
calcium handling↑ [39],
CM communication↑ [40, 41],
myofibrillar structural damage in response to ErbB inhibition [38] | Development of cardiac conduction system↑ [45, 46],
CM dedifferentiation and proliferation↑ [42, 43],
myofilament organization↑ [44] | cardiac output↑,
LVEF↑,
systemic vascular resistance↓,
ESV↓ EDV↓ [50, 51] |
|
| Follistatin-like 1 (Fstl1) | DIP2A (disconnected interacting protein 2 homolog A) | ① AMPK↑ [57]
② p-AKT↑ [58]
③ ERK1/2↑ [55] | Cell apoptosis↓ [58] | Cardiac rupture↓ [55],
CM proliferation↑, heart performance↑ [56] | N/A |
|
| TNF-related weak inducer of apoptosis (TWEAK) | Fn14 receptor | ① TRAFNF-κB↑ [68]
② ERK [70]
③ PI3KAKT↑ [70] | CM cell cycle reentry↑ [70],
cardiomyocyte proliferation↑ [69],
CM-derived proinflammatory cytokines↑ [68],
fibroblast proliferation and myofibroblast differentiation↑ [71] | Cardiac hypertrophy↑ [72],
myocardial inflammatory responses↑ [73],
heart performance↓ [74] | N/A |
|
