Cardiac hypertrophy is a main contributor to heart failure, where therapeutic options are limited. Increasing evidence exists regarding up-regulation of histone lysine-specific demethylase 4A (KDM4A) in patients with cardiac hypertrophy as a risk factor, although the mechanisms behind are not well understood.

Calcific aortic valve disease (CAVD) is the most prevalent acquired valve heart disorder in aging populations. Its most severe form in aortic valve stenosis (AVS), with an average survival of 2-3 years once symptoms appear. The early diagnosis of AVS based on circulating biomarkers is crucial to label high-risk patients before they progress to the severe form.

Vasthera Co. Ltd. has received IND clearance from the U.S. FDA, enabling it to initiate a phase I trial for VTB-10 for pulmonary arterial hypertension (PAH). Vasthera identified a deficiency of the enzyme peroxiredoxin (PRX) in PAH lesions and used its Redoxizyme platform to develop VTB-10, a small-molecule enzyme that precisely replicates PRX function.

Eukaryotic translation initiation factor 2-α kinase 3 (PERK) plays a role in homeostasis maintenance of the mitochondria-associated membrane (MAM), which in turn has an impact on the mitochondrial energy metabolism and structural morphology. To date, there is still controversy regarding the therapeutic effect of activating PERK for ischemia-reperfusion injury (I/R) management.

Although congenital aortic valve disease (AVD) is one of the most prevalent types of congenital heart disease, affecting 1% to 2% of the population, the understanding of the molecular genetics and mechanisms underlying the disease remains limited.

Endoplasmic reticulum oxidoreductase 1 (ERO1) has traditionally been associated with proper protein folding in the endoplasmic reticulum, but it has recently been linked to platelet activation and aggregation in arterial thrombosis and ischemic stroke.