Scientists from Osaka University, in their recent Hypertension paper, investigated ways to prevent cardiac failure from AMI, focusing on periostin, a group of extracellular matrix proteins (Gene ID).
After AMI starts to develop, fibroblasts secrete periostin to heal and regenerate damaged tissue. However, the team from Osaka confirmed that “cell adhesion inhibition” of periostin1 actually causes damage to myocardial cells, promotes myocyte death, and exacerbates the conditions leading to heart failure.
A treatment that inhibits periostin proteins seemed to be the answer to reducing heart failure risk, but the results from that treatment were twofold. Without periostin1, heart failure following AMI was suppressed, but death from cardiac rupture following AMI increased.
The team from Osaka identified this effect as a result of differing functions among periostin variants. While periostin1 leads to cardiac failure outcomes, periostin2 and periostin4 actually have cardioprotective effects:
- Myocardial regeneration
- Angiogenesis
- Protection from cardiac rupture after AMI
This new therapeutic method provides patients with an improved quality of life as well as decreases medical spending on cardiac failure treatment.
Source: Osaka University