Both Ghrelin and Its Inactive Form Des-Acyl Ghrelin Protect Heart and Blood Vessel Cells From Death
Both acylated ghrelin and its des-acyl form (which doesn't activate the classical GHS receptor) protected cardiomyocytes and endothelial cells from apoptosis through ERK1/2 and PI3K/Akt survival pathways — a GHS-R independent mechanism.
Quick Facts
What This Study Found
Both acylated ghrelin and des-acyl ghrelin inhibited apoptosis in cardiomyocytes and endothelial cells via ERK1/2 and PI3K/Akt pathways, with des-acyl ghrelin's activity demonstrating GHS-R-independent cardiovascular protection.
Key Numbers
How They Did This
In-vitro study. Cultured cardiomyocytes and endothelial cells exposed to serum starvation or doxorubicin to induce apoptosis. Both ghrelin forms tested for survival signaling (ERK1/2, PI3K/Akt) and apoptosis inhibition.
Why This Research Matters
Des-acyl ghrelin is the most abundant form in blood. If it protects the heart independently of the GHS receptor, it represents a major, previously unrecognized cardiovascular protective system with its own unknown receptor.
The Bigger Picture
Des-acyl ghrelin was considered an inactive waste product. This study reveals it's actually a cardiovascular protective molecule working through its own receptor — a major paradigm shift in ghrelin biology.
What This Study Doesn't Tell Us
In-vitro cell culture study. The des-acyl ghrelin receptor has not been identified. In-vivo cardioprotective significance not established.
Questions This Raises
- ?What is the receptor for des-acyl ghrelin's cardiovascular effects?
- ?Does circulating des-acyl ghrelin protect the heart in vivo?
- ?Could des-acyl ghrelin be developed as a cardioprotective drug without GH/appetite side effects?
Trust & Context
- Key Stat:
- Inactive form active! Des-acyl ghrelin — previously considered inactive — protects heart cells through its own receptor, separate from the classical ghrelin receptor
- Evidence Grade:
- Moderate in-vitro evidence with clear mechanistic pathway identification and the novel finding of GHS-R-independent activity.
- Study Age:
- Published in 2002. Des-acyl ghrelin's biological activities have been further confirmed, with ongoing search for its specific receptor.
- Original Title:
- Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyocytes and endothelial cells through ERK1/2 and PI 3-kinase/AKT.
- Published In:
- The Journal of cell biology, 159(6), 1029-37 (2002)
- Authors:
- Baldanzi, Gianluca, Filigheddu, Nicoletta, Cutrupi, Santina, Catapano, Filomena, Bonissoni, Sara, Fubini, Alberto, Malan, Daniela, Baj, Germano, Granata, Riccarda, Broglio, Fabio, Papotti, Mauro, Surico, Nicola, Bussolino, Federico, Isgaard, Jorgen, Deghenghi, Romano, Sinigaglia, Fabiola, Prat, Maria, Muccioli, Giampiero, Ghigo, Ezio, Graziani, Andrea
- Database ID:
- RPEP-00712
Evidence Hierarchy
Frequently Asked Questions
What is des-acyl ghrelin?
Most ghrelin in your blood lacks the fatty acid tag needed to activate the hunger/GH receptor. This 'des-acyl' form was thought to be inactive, but this study shows it protects heart cells through its own separate pathway.
Could this become a heart drug?
Potentially. Since des-acyl ghrelin doesn't activate the hunger receptor, it could protect the heart without causing increased appetite or GH release — a 'clean' cardioprotective agent.
Read More on RethinkPeptides
Cite This Study
https://rethinkpeptides.com/research/RPEP-00712APA
Baldanzi, Gianluca; Filigheddu, Nicoletta; Cutrupi, Santina; Catapano, Filomena; Bonissoni, Sara; Fubini, Alberto; Malan, Daniela; Baj, Germano; Granata, Riccarda; Broglio, Fabio; Papotti, Mauro; Surico, Nicola; Bussolino, Federico; Isgaard, Jorgen; Deghenghi, Romano; Sinigaglia, Fabiola; Prat, Maria; Muccioli, Giampiero; Ghigo, Ezio; Graziani, Andrea. (2002). Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyocytes and endothelial cells through ERK1/2 and PI 3-kinase/AKT.. The Journal of cell biology, 159(6), 1029-37.
MLA
Baldanzi, Gianluca, et al. "Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyocytes and endothelial cells through ERK1/2 and PI 3-kinase/AKT.." The Journal of cell biology, 2002.
RethinkPeptides
RethinkPeptides Research Database. "Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyo..." RPEP-00712. Retrieved from https://rethinkpeptides.com/research/baldanzi-2002-ghrelin-and-desacyl-ghrelin
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkPeptides research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.