Building and Repairing the Heart: What Can We Learn from Embryonic Development?

Table 1

Overview of studies targeting different signaling pathways in heart pathological stress.

Pathway	Affected member	Effect	References
Notch	notch1 (⊣)	Increased hypertrophy, fibrosis, and mortality; impaired adult CPCs commitment into myocytic lineage	[38, 39]
	notch1 (→)	Improved wall thickness and cardiac function; enhanced neovascularization; decreased infarct area	[40, 41]
	jagged1 (→)	Restraint of myocardial hypertrophy and fibrosis; increased CPCs proliferation	[42]
FGF	FGF1 (→); FGF2 (→)	Preserved wall thickness; reduced scaring; improved cardiac function; increased proliferation and angiogenesis; increased CM viability	[43, 44]
SHH	Shh (→)	Restoration of LV function in acute and chronic ischemia; enhanced neovascularization; reduced fibrosis and apoptosis	[45]
	SHH-heparin complexes (→)	Production of survival factors; attenuation of CM apoptosis	[46]
Wnt/𝛽-catenin	sFrp1 (→)	Prevented CM apoptosis; antifibrotic effect	[47–49]
	SFRP2 (→)
	dishevelled (→)	Myocardial hypertrophy; severe cardiomyopathy	[50]
TGF/BMP	SMAD6 (⊣)	Increased cell proliferation; hyperplastic cardiac cushions	[51, 52]
	noggin (⊣)
	Bambi (⊣)	Hypertrophy; chamber dilation; deterioration of systolic function; diastolic dysfunction	[53]
	Tgfb1 (→)	Cardiac hypertrophy; increased interstitial fibrosis	[54]

(⊣) Inhibition or (→) activation of the specific pathway member.