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首页> 外文期刊>Journal of Neuroscience and Behavioral Health >Is the age-related macular degeneration (AMD) vascular disease, part of vasculopathy, respectively? Novel considerations on AMD arising from the newest pathophysiological, clinical and clinical-pharmacological observations (Preliminary Communication)
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Is the age-related macular degeneration (AMD) vascular disease, part of vasculopathy, respectively? Novel considerations on AMD arising from the newest pathophysiological, clinical and clinical-pharmacological observations (Preliminary Communication)

机译：与年龄相关的黄斑变性（AMD）血管疾病分别是血管病变的一部分吗？最新的病理生理学，临床和临床药理学观察结果引起的关于AMD的新考虑（初步交流）

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In the genesis and later development of age-related macular degeneration (AMD), endothelial dysfunction (ED) has a crucial role. AMD-risk factors, which play a decisive role in AMD, are in a close connection, correlate with, and often are identical wih the risk factors (RFs) of cardiovascular diseases (CVDs), so that it can reasonably be presumed that the two conditions have a similar pathogenesis. These risk factors, which seem essentially different, lead to chronic vascular injury based on the same mechanism of action: by inducing oxidative stress (OS). ED itself is a consequential-consecutive phenomenon (OS→ED!), and is a clinico-pathophysiologically important connecting link between harm(s)oxa and vascular injury (harm [noxa] → oxidative stress (OS) → endothelial activation (EA), endothelial dysfunction (ED), respectively → vacular injury, vascular disease). Disordered function of endothelium in the vessels supplying the affected ocular structures with blood (ED) have a key role in the genesis and development of age-related macular degeneration. Changes in blood vessels including those in choroids may be triggered by several repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic, and genetic influences/impactsoxa (in fact, the risk factors!), against which protracted response[1]**) (increased ROS formation → oxidative stress → endothelial activation/dysfunction → aftermath of EA/ED) may develop, and in consequence of this, (chronic) vascular damage (functional and then structural alteration [remodelling] of the blood vessel), pathological consecutive changes ending in AMD, ultimately, may develop (choriocapillaris degenerates in exudative AMD, choriocapillaris degeneration precedes retinal pigment epithelial atrophy in wet AMD). All this goes to show that AMD may be a local manifestation of systemic (vascular) disease, undoubtedly. AMD is the disease of the aging body. Normal aging processes can lead to structural and blood flow changes that can predispose patients to AMD. Advancing age is a privotal and independent risk factor for vascular disease as can be understood from the fact that aging individuals often demonstrate dysfunctional blood vessel repair after vascular injury and aging per se, in the absence of other risk factors is associated with oxidativeitrosative stress and inflammatory?changes in the phenotype of blood vessels (primary abnormalities in ocular perfusion worsen with age, secondarily causing dysfunction of the retinal pigment epithelial cells, predisposing eyes to AMD), these changes together with individual’s (environmental) risk factors set the stage for the development of AMD. Regarding therapy/preventive treatment/prevention of AMD: (I) Non-medicinal (preventive) treatment such as lifestyle modifications of AMD patients (modifying lifestyles behavours of diet, smoking and physical activity) is of indispensable importance; they influence strongly and very beneficially the established vascular?risk factors and also advantageously affect novel pathways of risk such as?inflammation/oxidative stress, endothelial function, thrombosis/coagulation. Modest alterations of these lifestyle?risk factors are achievable and have substantial effects on?(vascular) risk. (II) Various medicaments: (1) ACE inhibitors, (2) AR blockers [including telmisartan with its peroxisome proliferator-activated receptor-gamma |PPARgamma| agonist effect], (3) statins, (4) acetylsalicylic acid, (5) trimetazidine, (6) third generation beta blockers, and (7) PPARgamma agonists, exert a beneficial effect on endothelial dysfunction and its consequential functional, structural and metabolic disorders. The advantageous/beneficial effect of a favourable influence on the successful treatment of ED in patients with chronic vascular and cardiovascular diseases has become evidence now, as the human vascular system is uniform, consubstantial thus medicines beneficial in ED may exert a favourable effect also on the vessels of the eye, in the retina/choroid (per analogiam of cardiovascular disease). The antioxidant vitamins (AOVs) used for preventing OS, conventionally, did not really live up to the hopes placed in them. The activity of AOVs against OS is limited only to scavenging the already formed oxidative products: the inhibition of the reaction pathway peroxynitrite → DNA damage → PARP by rapid catalytic breakdown of peroxynitrite with the help of the so-called?"causal"antioxidants with mitochondrial effects (FP15 metalloporphyrin compound), showing great promise, or by the inhibition of PARP with INO-100 may open a new possibility in the treatment of OS induced vascular dysfunction in several pathologic conditions including AMD.- Nevertheless, we have excellent therapeutic possibilities/options also, until then: the statins, the ACEIs, ARBs, ASA, the trimetazidin, third generation beta-blockers, PPARgamma agonists. As the human vascular system is uniform and consubstantial, thus m
机译：在年龄相关性黄斑变性（AMD）的发生和后期发展中，内皮功能障碍（ED）发挥着至关重要的作用。在AMD中起决定性作用的AMD危险因素与心血管疾病（CVD）的危险因素（RF）密切相关，相互关联且经常是相同的，因此可以合理地推测这两者病情有相似的发病机理。这些危险因素似乎本质上不同，它们基于相同的作用机理导致慢性血管损伤：诱导氧化应激（OS）。 ED本身是一种连续的现象（OS→ED！），并且是伤害/诺沙与血管损伤（伤害[诺沙]→氧化应激（OS）→内皮激活（EA））之间在临床病理生理上重要的联系），内皮功能障碍（ED）→血管损伤，血管疾病）。在向受影响的眼部结构供血（ED）的血管中，内皮功能紊乱在与年龄有关的黄斑变性的发生和发展中起着关键作用。反复发生和/或长时间的机械，物理，化学，微生物学，免疫学和遗传学影响/影响/诺沙（实际上是危险因素！）可能会触发血管变化，包括脉络膜血管的变化，从而延长响应时间[ 1] **）（ROS形成增加→氧化应激→内皮活化/功能异常→EA / ED的后果），因此，（慢性）血管损伤（血液的功能性和结构性改变[重塑]）血管），最终可能会发生以AMD结束的病理性连续变化（渗出性AMD中脉络膜毛细血管变性，湿性AMD中脉络膜毛细血管变性在视网膜色素上皮萎缩之前）。所有这些都表明，毫无疑问，AMD可能是全身性（血管）疾病的局部表现。 AMD是衰老的身体疾病。正常的衰老过程会导致结构和血流变化，从而使患者更易患AMD。可以理解，年龄增长是血管疾病的一个独立的，独立的危险因素，可以从以下事实中了解到：在没有其他危险因素的情况下，衰老的个体通常在血管损伤和衰老后本身就表现出功能失调的血管修复与氧化/亚硝化应激有关。以及血管表型的炎症变化（眼灌注的主要异常随着年龄的增长而恶化，其次导致视网膜色素上皮细胞功能异常，使眼睛易患AMD），这些变化以及个体（环境）的危险因素共同为疾病的发展奠定了基础。 AMD的发展。关于AMD的治疗/预防性治疗/预防：（I）非药物性（预防性）治疗，例如改变AMD患者的生活方式（改变饮食，吸烟和体育锻炼的生活方式）至关重要。它们强烈且非常有益地影响已建立的血管危险因素，并且还有利地影响新的危险途径，例如炎症/氧化应激，内皮功能，血栓形成/凝血。这些生活方式风险因素的适度改变是可以实现的，并且对（血管）风险具有实质性影响。 （II）多种药物：（1）ACE抑制剂，（2）AR阻滞剂[包括替米沙坦及其过氧化物酶体增殖物激活的受体-γ| PPARg |激动剂]，（3）他汀类药物，（4）乙酰水杨酸，（5）曲美他嗪，（6）第三代β受体阻滞剂和（7）PPARγ激动剂对内皮功能障碍及其功能，结构和代谢产生有益作用失调。对慢性血管和心血管疾病患者成功治疗ED的有利影响的有益/有益作用现已成为证据，因为人的血管系统是均匀的，因此大量有益于ED的药物也可能对ED产生有利的作用。视网膜/脉络膜中的眼睛血管（根据心血管疾病的类似情况）。传统上，用于预防OS的抗氧化剂维生素（AOV）并没有真正实现它们的希望。 AOV对OS的活性仅限于清除已经形成的氧化产物：通过过氧化亚硝酸盐与所谓的“因果”抗氧化剂与线粒体的快速催化分解，抑制过氧化亚硝酸盐→DNA损伤→PARP的反应途径效果（FP15金属卟啉化合物），显示出广阔的前景，或通过用INO-100抑制PARP可能为OS诱发的某些病理状况（包括AMD）引起的血管功能障碍开辟新的可能性。-然而，我们有出色的治疗可能性/直到那时还可以选择：他汀类药物，ACEI，ARB，ASA，曲美他汀，第三代β受体阻滞剂，PPARγ激动剂。由于人体血管系统是均匀而实质的，因此

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