Haibao Shang

TL;DR: It is shown that receptor-interacting protein 3 (RIP3) triggers myocardial necroptosis, in addition to apoptosis and inflammation, through activation of Ca2+-calmodulin–dependent protein kinase (CaMKII) rather than through the well-established RIP3 partners RIP1 and MLKL.

TL;DR: It is shown that a protein kinase D2 (PRKD2) nonsense mutation (K410X) in two rhesus monkeys with extreme hyperinsulinemia along with IR and metabolic defects is identified by using extreme phenotype sampling and deep sequencing analyses, indicating that down-regulation of PRKD1 is involved in the pathogenesis of hyperinsulainemia which, in turn, results in IR and metabolism disorders.

TL;DR: It is demonstrated that CaMKII-δ9 inhibition with knockdown or knockout of its feature exon, exon 16, protects the heart against I/R-elicited injury and subsequent heart failure, providing a novel therapeutic strategy for various ischemic heart diseases.

TL;DR: These findings not only suggest that hesperadin is a promising leading compound for clinical therapy of cardiac I/R injury and heart failure, but also provide a strategy for the joint therapy of cancer and cardiovascular disease caused by anticancer treatment.

TL;DR: A non-human primate model with spontaneous RA similar to the human conditions identified that RIPK1-VDAC1 pathway is a promising target to treat cardiac impairment in RA.