Cardiomyocyte-derived C-type natriuretic peptide diminishes myocardial ischaemic injury by promoting revascularisation and limiting fibrotic burden
Cardiomyocytes synthesize and release CNP as an intrinsic protective mechanism in response to MI that reduces cardiac structural and functional deficits; these salutary actions are primarily NPR-C-dependent. Pharmacological targeting of CNP may represent a new therapeutic option for MI.
Authors
- Aisah A. Aubdool (ORCID: https://orcid.org/0000-0002-4712-9421)
- Reshma S. Baliga (ORCID: https://orcid.org/0000-0002-5582-5152)
- Nicola Smart (ORCID: https://orcid.org/0000-0002-3501-7254)
- Joshua P. Dignam (ORCID: https://orcid.org/0000-0003-1826-6336)
- Cristina Pérez‐Ternero (ORCID: https://orcid.org/0000-0002-2349-0642)
- Adrian J. Hobbs (ORCID: https://orcid.org/0000-0002-3589-7108)
- Amie J. Moyes (ORCID: https://orcid.org/0000-0001-9336-9904)
- Vanessa J. Lowe
Institutions
- Queen Mary University of London (GB)
- University of Oxford (GB)
- William Harvey Research Institute (GB)
Publication Details
- Journal
- Pharmacological Research
- Published
- 2024-10-05
- DOI
- https://doi.org/10.1016/j.phrs.2024.107447
- Citations
- 1
- Primary Topic
- Cardiac Fibrosis and Remodeling
- Type
- article
- Field-Weighted Citation Impact
- 0.40
Funders
- British Heart Foundation