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.
Shire Human Genetic Therapies Inc. has discovered new plasma kallikrein (KLKB1) inhibitors reported to be useful for the treatment of hereditary angioedema and diabetic macular edema.
Researchers from the International Centre for Genetic Engineering and Biotechnology and colleagues have worked on the systematic identification of cellular proteins that can exert cardioprotective activity after a myocardial infarction (MI).
Zhejiang University has disclosed transient receptor potential cation channel subfamily M member 2 (TRPM2) antagonists reported to be useful for the treatment of stroke and ischemia-reperfusion injury, among others.
Researchers from the University of California and affiliated organizations have published data from a study that focused on screening of factors involved in hepatic low-density lipoprotein receptor (LDLR) regulation, with the aim of identifying potential new therapeutic targets in cardiovascular disease.
Ambulero Inc., a spinout from the University of Miami Miller School of Medicine, has received a positive response from a type B pre-IND meeting with the FDA on the development of AMB-301 as a treatment for the vascular disease Buerger's disease.
The coagulation factor XI (FXI) from the liver acts as an endocrine molecule in the heart, protecting it from heart failure. Scientists at the University of California, Los Angeles (UCLA) found that this communication between the two organs is mediated by the interaction between FXI and a heart protein. This interaction activated genes in cardiomyocytes that reduced inflammation, fibrosis and diastolic dysfunction, protecting the heart from a heart attack. That FXI participates in preventing heart failure suggests the possibility of using it as a therapeutic target.
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