AI Article Synopsis
- Natriuretic peptides produced by the stressed heart help reduce cardiac workload through vasodilation, natriuresis, and diuresis, providing a basis for new heart-failure treatments.
- Researchers discovered that zDHHC9 palmitoylates Rab3gap1, which alters its relationship with Rab3a, leading to increased levels of Rab3a-GTP and issues with exocytosis.
- This new understanding of the mechanisms behind natriuretic peptide release could lead to innovative strategies for enhancing heart failure therapies.
Article Abstract
Production and release of natriuretic peptides by the stressed heart reduce cardiac workload by promoting vasodilation, natriuresis, and diuresis, which has been leveraged in the recent development of novel heart-failure pharmacotherapies, yet the mechanisms regulating cardiomyocyte exocytosis and natriuretic peptide release remain ill defined. We found that the Golgi S-acyltransferase zDHHC9 palmitoylates Rab3gap1 resulting in its spatial segregation from Rab3a, elevation of Rab3a-GTP levels, formation of Rab3a-positive peripheral vesicles, and impairment of exocytosis that limits atrial natriuretic peptide release. This novel pathway potentially can be exploited for targeting natriuretic peptide signaling in the treatment of heart failure.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10264568 | PMC |
| http://dx.doi.org/10.1016/j.jacbts.2022.11.003 | DOI Listing |
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