FLT4 causes developmental disorders of the cardiovascular and lymphovascular systems via pleiotropic molecular mechanisms.
Richard M MonaghanRichard W NaylorDaisy FlatmanPaul R KasherSimon G WilliamsBernard D KeavneyPublished in: Cardiovascular research (2024)
Proteostatic dysfunction, if confirmed as a mechanism of CHD pathogenesis for other predisposing genes, may identify pathways to therapeutic interventions. Distinguishing mechanistically how variants in FLT4 give rise to CHD may have potential to individualise genetic counselling in affected families.
Keyphrases
- acute myeloid leukemia
- genome wide
- copy number
- tyrosine kinase
- physical activity
- oxidative stress
- dna methylation
- lymph node metastasis
- endometrial cancer
- smoking cessation
- human health
- bioinformatics analysis
- hiv testing
- genome wide identification
- transcription factor
- gene expression
- risk assessment
- antiretroviral therapy