Why the study?
The human BDNF Val66Met single nucleotide polymorphism has recently been linked to an increased propensity for arterial thrombosis related to acute myocardial infarction.
Does the BDNF Val66Met polymorphism worsen cardiac remodeling and alter macrophage phenotype after myocardial infarction?
Population
BDNFVal66Met homozygous mutant and wild-type mice undergoing LAD coronary artery ligation, and patients with coronary heart disease
Comparison
BDNFMet/Met versus BDNFVal/Val
Design
Preclinical animal and translational in vitro study
Authors
Loading...
May elevate post-AMI thrombosis risk in carriers; leaves open clinical translation from mouse models.
Does the BDNF Val66Met polymorphism worsen cardiac remodeling and alter macrophage phenotype after myocardial infarction?
The BDNF Val66Met polymorphism predisposes to adverse cardiac remodeling post-myocardial infarction by promoting a pro-inflammatory macrophage phenotype, providing a novel cellular mechanism for its associated cardiovascular risk.
Sandrini et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: