LMNA gene mutations are the second most common cause of genetic dilated...

Increased expression and elevated levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 play a role in impaired cardiac function. These MMPs make for essential targets in the treatment of heart failure, specifically heart failure with preserved ejection fraction (HFpEF).

Calcium/calmodulin-dependent protein kinase II (CaMKII) is involved in the regulation of calcium and its hyperactivation can lead to cardiac issues, particularly with rhythm and contraction.

AMPK activation improves cardiac function in multiple ways, from regulating lipid and glucose to directly protecting cardiac cells.

Myocardial infarction, a result of uncontrolled heart disease, often results in death.

As they matured from prenatal to adult, heart cells reduced the number of nuclear pores by more than 60%. That decrease protected them from the consequences of stress, but also impaired their ability to regenerate. “These findings are an important advance in fundamental understanding of how the heart develops with age and how it has evolved to cope with stress,” senior author Bernhard Kühn, professor of pediatrics and director of the Pediatric Institute for Heart Regeneration and Therapeutics at the University of Pittsburgh School of Medicine, said in a press release. Kühn and his colleagues published those findings in the Oct. 24, 2022, issue of Developmental Cell.

Vivasc Therapeutics Inc. has initiated work under a second National Institutes of Health (NIH) phase I STTR research grant, in conjunction with Georgetown University.