Key result
Overexpression of CLEC3B increased cell viability (P<0.01) and inhibited apoptosis (P<0.05) in hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.
Why the study?
Serum levels of CLEC3B are downregulated in cardiovascular disease, but the molecular mechanisms of CLEC3B in ischemic heart disease are not well-characterized.
Population
H9c2 rat cardiomyocytes cultured under oxygen-deficit conditions
Comparison
CLEC3B overexpression vs CLEC3B silencing
Design
In vitro controlled laboratory study
Authors
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CLEC3B may protect hypoxic cardiomyocytes; animal data leave open its viability as an ischemic heart disease target.
p-value: p=<0.01
CLEC3B protects H9c2 cardiomyocytes from hypoxia-induced apoptosis via activation of the PI3K/Akt pathway, suggesting a potential molecular target for ischemic heart disease.
Lv et al. (2020) studied Ischemic heart disease (in vitro model). CLEC3B overexpression and silencing vs. Hypoxic H9c2 cardiomyocytes without CLEC3B modification was evaluated on Cell viability and apoptosis (p=<0.01). Overexpression of CLEC3B increased cell viability (P<0.01) and inhibited apoptosis (P<0.05) in hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.
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