Oxidative stress: dual pathway induction in cardiorenal syndrome type 1 pathogenesis.
Oxidative stress: dual pathway induction in cardiorenal syndrome type 1 pathogenesis.
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DOI：
10.1155/2015/391790
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发表时间：
2015
影响因子：
--
通讯作者：
Ronco C
中科院分区：
文献类型：
--
作者：
Virzì GM;Clementi A;de Cal M;Brocca A;Day S;Pastori S;Bolin C;Vescovo G;Ronco C
心肾综合征1型(Type 1)是一种特殊的疾病，其特征是心功能迅速恶化，导致急性肾损伤(AKI)。尽管其病理生理机制复杂，目前仍未完全了解，但氧化应激似乎发挥了关键作用。在这项研究中，我们研究了氧化应激在CRS 1型发病机制中的可能作用。23名急性心力衰竭(AHF)患者参与了这项研究。对11例AHF并发AKI的患者进行血清IL-6、髓过氧化物酶(MPO)、一氧化氮(NO)、铜/锌超氧化物歧化酶(铜/锌超氧化物歧化酶)及内源性过氧化物酶活性(EPA)的定量检测。CRS 1型患者外周血中ROS和RNS显著升高，IL-6表达明显增强。所有氧化应激标志物的定量分析显示，与CRS 1型患者相比，对照组和AHF患者的氧化应激水平显著降低(P<；0.05)。这项先导性研究表明，与AHF患者相比，CRS 1型患者中双重氧化应激途径的诱导显著增加。我们的发现表明，氧化应激是一个潜在的治疗靶点，因为它通过ROS/RNS相关的发病机制促进炎症。
Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (P < 0.05). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.
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影响因子：
37.8
作者：
Baldus, S;Heeschen, C;Hamm, CW
通讯作者：
Hamm, CW
DOI：
10.1159/000142934
发表时间：
2008
期刊：
Nephron. Experimental nephrology
影响因子：
--
作者：
Kinsey GR;Li L;Okusa MD
通讯作者：
Okusa MD
影响因子：
7.4
作者：
Gill, Roop;Tsung, Allan;Billiar, Timothy
通讯作者：
Billiar, Timothy
影响因子：
13.6
作者：
Kielar, ML;John, R;Lu, CY
通讯作者：
Lu, CY
影响因子：
16.2
作者：
通讯作者：
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