2. Academic Validation
  3. Interleukin-33 induces angiogenesis after myocardial infarction via AKT/eNOS signaling pathway

Interleukin-33 induces angiogenesis after myocardial infarction via AKT/eNOS signaling pathway

  • Int Immunopharmacol. 2024 Dec 25;143(Pt 3):113433. doi: 10.1016/j.intimp.2024.113433.
Jiaqi Yu 1,  Yuyu Li 2,  Jiaxin Hu 3,  Yuan Wang 4
Affiliations

Affiliations

  • 1 Beijing Anzhen Hospital, Capital Medical University, Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Collaborative Innovation Centre for Cardiovascular Disorders, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China; Beijing Institute of Heart, Lung and Blood Vessel Disease, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China. Electronic address: yujiaqi_@mail.ccmu.edu.cn.
  • 2 Beijing Anzhen Hospital, Capital Medical University, Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Collaborative Innovation Centre for Cardiovascular Disorders, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China; Beijing Institute of Heart, Lung and Blood Vessel Disease, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China.
  • 3 Cardiovascular Disease Center, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei, China; Hubei Selenium and Human Health Institute, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi 445000, China.
  • 4 Beijing Anzhen Hospital, Capital Medical University, Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Collaborative Innovation Centre for Cardiovascular Disorders, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China; Beijing Institute of Heart, Lung and Blood Vessel Disease, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China. Electronic address: wangyuan980510@ccmu.edu.cn.
PMID: 39486188 DOI: 10.1016/j.intimp.2024.113433
Abstract

Myocardial infarction (MI) is one of the leading causes of mortality and morbidity worldwide. MI-damaged vascular structures are difficult to completely restore due to the heart's low regenerative capacity. Given interleukin-33 (IL-33) as a potent endothelial activator promoting angiogenesis, this study investigated the role of IL-33 in angiogenesis and cardiac repair after MI. A mouse model of MI was established. IL-33 improved cardiac function and induced an increase in vascular density after MI. Besides, IL-33 promoted human endothelial cells proliferation, migration, and differentiation under both normoxic and hypoxic conditions, consistently with increased angiogenesis in vivo. Mechanistic studies demonstrated that IL-33 could promote angiogenesis by activating eNOS and Akt, and stimulating NO production in vivo and in vitro. Given that injection of exogenous IL-33 induced an inflammatory response, we employed a multifunctional biomimetic nanoparticle drug delivery system to deliver IL-33, thereby enhancing its targeting to the heart for fibrotic therapy and reducing inflammation. In conclusion, our results indicate that IL-33 promotes endothelial angiogenesis after MI through Akt/eNOS/NO signaling pathway. PM&EM/IL-33 nanoparticles may hold promising therapeutic potential for protecting cardiac ischemic injury and mitigating inflammation.

Keywords

Angiogenesis; Endothelial cells; Inflammation; Interleukin-33; Myocardial infarction; Nanoparticle delivery system.

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