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TGFβ-Neurotrophin Interactions in Heart, Retina, and Brain
Biomolecules ( IF 5.5 ) Pub Date : 2021-09-14 , DOI: 10.3390/biom11091360
Anja Schlecht 1 , Mario Vallon 1 , Nicole Wagner 1 , Süleyman Ergün 1 , Barbara M Braunger 1
Affiliation  

Ischemic insults to the heart and brain, i.e., myocardial and cerebral infarction, respectively, are amongst the leading causes of death worldwide. While there are therapeutic options to allow reperfusion of ischemic myocardial and brain tissue by reopening obstructed vessels, mitigating primary tissue damage, post-infarction inflammation and tissue remodeling can lead to secondary tissue damage. Similarly, ischemia in retinal tissue is the driving force in the progression of neovascular eye diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD), which eventually lead to functional blindness, if left untreated. Intriguingly, the easily observable retinal blood vessels can be used as a window to the heart and brain to allow judgement of microvascular damages in diseases such as diabetes or hypertension. The complex neuronal and endocrine interactions between heart, retina and brain have also been appreciated in myocardial infarction, ischemic stroke, and retinal diseases. To describe the intimate relationship between the individual tissues, we use the terms heart-brain and brain-retina axis in this review and focus on the role of transforming growth factor β (TGFβ) and neurotrophins in regulation of these axes under physiologic and pathologic conditions. Moreover, we particularly discuss their roles in inflammation and repair following ischemic/neovascular insults. As there is evidence that TGFβ signaling has the potential to regulate expression of neurotrophins, it is tempting to speculate, and is discussed here, that cross-talk between TGFβ and neurotrophin signaling protects cells from harmful and/or damaging events in the heart, retina, and brain.

中文翻译:

TGFβ-神经营养因子在心脏、视网膜和大脑中的相互作用

对心脏和大脑的缺血性损伤,即心肌梗塞和脑梗塞,分别是全世界死亡的主要原因之一。虽然存在通过重新打开阻塞血管来允许缺血性心肌和脑组织再灌注的治疗选择,但减轻原发性组织损伤、梗塞后炎症和组织重塑可导致继发性组织损伤。同样,视网膜组织缺血是糖尿病视网膜病变 (DR) 和年龄相关性黄斑变性 (AMD) 等新生血管性眼病进展的驱动力,如果不及时治疗,最终会导致功能性失明。有趣的是,易于观察的视网膜血管可以用作心脏和大脑的窗口,以判断糖尿病或高血压等疾病中的微血管损伤。心脏、视网膜和大脑之间复杂的神经元和内分泌相互作用在心肌梗塞、缺血性中风和视网膜疾病中也得到了认可。为了描述个体组织之间的密切关系,我们在这篇综述中使用了术语心-脑和脑-视网膜轴,并着重于转化生长因子 β (TGFβ) 和神经营养因子在生理和病理条件下调节这些轴的作用. 此外,我们特别讨论了它们在缺血/新生血管损伤后炎症和修复中的作用。由于有证据表明 TGFβ 信号传导具有调节神经营养因子表达的潜力,因此很容易推测,并在此讨论,TGFβ 和神经营养因子信号传导之间的串扰可以保护细胞免受心脏、视网膜中的有害和/或破坏性事件的影响,
更新日期:2021-09-14
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