GLP-1RA therapy increases circulating vascular regenerative cell content in people living with type 2 diabetes

Author:

Park Brady1234ORCID,Krishnaraj Aishwarya1234ORCID,Teoh Hwee1235ORCID,Bakbak Ehab12346ORCID,Dennis Fallon1234ORCID,Quan Adrian123ORCID,Hess David A.23478ORCID,Verma Subodh12349ORCID

Affiliation:

1. Division of Cardiac Surgery, St. Michael’s Hospital, Unity Health Toronto, Toronto, Ontario, Canada

2. Keenan Research Centre for Biomedical Science, St Michael’s Hospital, Toronto, Ontario, Canada

3. Li Ka Shing Knowledge Institute, St Michael’s Hospital, Toronto, Ontario, Canada

4. Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada

5. Division of Endocrinology and Metabolism, St. Michael’s Hospital, Unity Health Toronto, Toronto, Ontario, Canada

6. Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia

7. Department of Physiology and Pharmacology, Western University, London, Ontario, Canada

8. Molecular Medicine Research Laboratories, Robarts Research Institute, London, Ontario, Canada

9. Department of Surgery, University of Toronto, Toronto, Ontario, Canada

Abstract

In this post hoc subanalysis of 92 individuals living with T2D and at high cardiovascular risk, the authors summarize the differences in circulating vascular regenerative (VR) progenitor cell content between those on GLP-1RA therapy, on SGLT2 inhibitor without GLP-1RA therapy, and on neither therapy. Those on GLP-1RA therapy demonstrated greater circulating VR progenitor cell content and reduced proinflammatory granulocyte precursor content. These results offer novel mechanistic insights into the cardiometabolic benefits associated with GLP-1RA therapy.

Funder

Canadian Government | Canadian Institutes of Health Research

Heart and Stroke Foundation of Canada

Publisher

American Physiological Society

Cited by 1 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Vascular regeneration: a new mechanism of glucagon-like peptide-1 receptor agonist-mediated cardioprotection?;American Journal of Physiology-Heart and Circulatory Physiology;2024-08-01

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