Review Article
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/-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] |
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) Inhibition or (→) activation of the specific pathway member.
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