Department of Biomedical Engineering, Tulane University , New Orleans, Louisiana.
Departmental of Biomedical Engineering, University of Florida , Gainesville, Florida.
J Appl Physiol (1985). 2018 Dec 1;125(6):1843-1850. doi: 10.1152/japplphysiol.00112.2018. Epub 2018 Apr 12.
Microvascular network growth and remodeling are common denominators for most age-related pathologies. For multiple pathologies (myocardial infarction, stroke, hypertension), promoting microvascular growth, termed angiogenesis, would be beneficial. For others (cancer, retinopathies, rheumatoid arthritis), blocking angiogenesis would be desirable. Most therapeutic strategies, however, are motivated based on studies using adult animal models. This approach is problematic and does not account for the impaired angiogenesis or the inherent network structure changes that might result from age. Considering the common conception that angiogenesis is impaired with age, a need exists to identify the causes and mechanisms of angiogenesis in aged scenarios and for new tools to enable comparison of aged versus adult responses to therapy. The objective of this article is to introduce opportunities for advancing our understanding of angiogenesis in aging through the discovery of novel cell changes along aged microvascular networks and the development of novel ex vivo models.
微血管网络的生长和重塑是大多数与年龄相关疾病的共同特征。对于许多疾病(心肌梗死、中风、高血压),促进微血管生长,即血管生成,将是有益的。对于其他疾病(癌症、视网膜病变、类风湿性关节炎),则希望阻断血管生成。然而,大多数治疗策略都是基于使用成年动物模型的研究而提出的。这种方法存在问题,因为它没有考虑到由于年龄导致的血管生成受损或固有网络结构变化。鉴于普遍认为血管生成随年龄而受损,因此需要确定衰老情况下血管生成的原因和机制,并需要新的工具来比较衰老和成年对治疗的反应。本文的目的是通过发现老年微血管网络中新型细胞变化和开发新型离体模型,为深入了解衰老过程中的血管生成提供机会。