Acute myocardial infarction (AMI) leads to lethal cardiac failure after oxygen depletion in the heart exceeds a “critical threshold” required for healthy cellular repair mechanisms. Without ample blood supply to the heart, heart cells either die or are damaged irreversibly (Cleveland Clinic
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
- Protection from cardiac rupture after AMI
Subsequently, their most successful treatment for preventing cardiac failure after AMI inhibited periostin1 without inhibiting periostin2 and periostin4. The treatment was developed with periostin variant-specific neutralizing antibodies.
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