Hexarelin attenuates abdominal aortic aneurysm formation by inhibiting SMC phenotype switch and inflammasome activation.
Jiang. Bo B; Wang. Mo M; Li. Xue X; Ren. Pengwei P; Li. Guangxin G; Wang. Yuqi Y; Wang. Lei L; Li. Xuan X; Yang. Dong D; Qin. Lingfeng L; Xin. Shijie S
Key Findings
- Hexarelin reduced the diameter of the abdominal aorta in mice with elastase‑induced aneurysms.
- It preserved elastin structure and maintained smooth‑muscle cell contractile markers (↑α‑SMA, ↓MMP2).
- Inflammation was dampened through inhibition of NF‑κB signaling, NLRP3 inflammasome activation, and lower IL‑18 levels.
Practical Outcomes
- The study suggests hexarelin may have protective effects on blood‑vessel health by curbing inflammation and preserving vessel wall integrity. However, the work was done in mice at a high dose, so there’s no clear guidance for safe or effective human use yet. More research is needed before biohackers consider adding hexarelin for cardiovascular or anti‑aging purposes.
Summary
In a mouse study, the growth‑hormone‑releasing peptide hexarelin helped prevent the widening of the abdominal aorta that leads to aneurysms. It kept the vessel wall's elastic fibers intact, kept smooth‑muscle cells in a healthy state, and lowered inflammation by blocking key immune pathways.
Abstract
Hexarelin, a synthetic growth hormone-releasing peptide, is shown to be protective in cardiovascular diseases such as myocardial infraction and atherosclerosis. However, the functional role of hexarelin in abdominal aortic aneurysm (AAA) remains undefined. The present study determined the effect of hexarelin administration (200 μg/kg twice per day) in a mouse model of elastase-induced abdominal aortic aneurysm. Echocardiography and in situ pictures showed hexarelin decreased infrarenal aorta diameter. Histology staining showed elastin degradation was improved in hexarelin-treated group. Hexarelin rescued smooth muscle cell contractile phenotype with increased α-SMA and decreased MMP2. Furthermore, hexarelin inhibited inflammatory cell infiltration, NLRP3 inflammasome activation and IL-18 production. Particularly, hexarelin suppressed NF-κB signaling pathway which is a key initiator of inflammatory response. These results demonstrated that hexarelin attenuated AAA development by inhibiting SMC phenotype switch and NF-κB signaling mediated inflammatory response.
Study Information
pubmed
2021
2021-11-29T00:00:00.000Z
10.1016/j.mvr.2021.104280
5
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