相关实验视频

Updated: Jun 8, 2025

Author Spotlight: Investigating Angiogenesis and Vessel Permeability Through a Modified Matrix Gel Plug Assay

Author Spotlight: Investigating Angiogenesis and Vessel Permeability Through a Modified Matrix Gel Plug Assay

Published on: June 30, 2023

介质素-33通过AKT/eNOS信号通路诱导心肌梗塞后的血管生成

Jiaqi Yu¹, Yuyu Li¹, Jiaxin Hu²

¹Beijing 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.

International immunopharmacology

|November 1, 2024

概括

介质素-33 (IL-33) 增强心肌梗塞 (MI) 后的血管形成和心脏修复. 通过促进血管生成和减少炎症,IL-33的纳米粒子输送显示了对心脏损伤的治疗潜力.

科学领域:

心血管研究研究心血管研究
再生医学是一种再生医学.
分子生物学分子生物学

背景情况:

心肌梗塞 (MI) 对全球死亡率和发病率作出了重大贡献.
心脏有限的再生能力阻碍了心脏中风后血管结构的完全恢复.
介质素-33 (IL-33) 被认为是促进血管生成的内皮激活剂.

研究的目的:

调查IL-33在促进血管生成和心脏中风后心脏修复方面的治疗潜力.
阐明IL-33影响血管生成的分子机制.
开发一种有效的IL-33输送系统,以减轻心脏缺血损伤和炎症.

主要方法:

建立了小鼠心肌梗塞 (MI) 的模型.
服用IL-33并评估心脏功能和血管密度.
利用体外试验测试来评估内皮细胞的增殖,迁移和分化.
研究了AKT/eNOS/NO信号通路.
开发并使用了一种多功能生物模拟纳米粒子药物递送系统,用于IL-33.

主要成果:

在MI小鼠模型中,IL-33的使用改善了心脏功能,并增加了血管密度.
在各种条件下,IL-33促进了人类内皮细胞的增殖,迁移和分化.
机械研究表明IL-33激活了AKT/eNOS/NO通路,增强了血管生成.
纳米颗粒传递的IL-33准了心脏,减少了炎症,并防止了缺血性损伤.

结论:

通过AKT/eNOS/NO信号通路,IL-33显著促进心脏病发作后的内皮血管生成.
携带IL-33的仿生纳米颗粒为心脏缺血损伤治疗和减少炎症提供了一个有希望的策略.

关键词:

血管新生的产生.内皮细胞是内皮细胞.炎症炎症是一种炎症.介质素-33 介质素-33 心肌梗塞的心脏病发作纳米粒子输送系统提供系统.

更多相关视频

In Vitro Model of Coronary Angiogenesis

In Vitro Model of Coronary Angiogenesis

Published on: March 10, 2020

A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision

A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision

Published on: May 13, 2021

相关概念视频

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...

Mechanism of Angiogenesis

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

Intracellular Signaling Affects Focal Adhesions

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Myocarditis III: Medical Management

Myocarditis III: Medical Management

Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...

Myocarditis I: Introduction

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...