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酒精滥用与肾损伤:流行病学证据及潜在机制

Alcohol Misuse and Kidney Injury: Epidemiological Evidence and Potential Mechanisms.

作者信息

Varga Zoltan V, Matyas Csaba, Paloczi Janos, Pacher Pal

机构信息

Zoltan V. Varga, M.D., Ph.D., is a visiting Research Fellow; Csaba Matyas, M.D., is a visiting Research Fellow; Janos Paloczi, Ph.D., is a visiting Research Fellow; and Pal Pacher, M.D., Ph.D., is a Senior Investigator and Lab Chief, all in the Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.

出版信息

Alcohol Res. 2017;38(2):283-288.

Abstract

Chronic alcohol consumption is a well-known risk factor for tissue injury. The link between alcohol use disorder (AUD) and kidney injury is intriguing but controversial, and the molecular mechanisms by which alcohol may damage the kidneys are poorly understood. Epidemiological studies attempting to link AUD and kidney disease are, to date, inconclusive, and there is little experimental evidence directly linking alcohol consumption to kidney injury. However, studies conducted primarily in other organs and tissues suggest several possible mechanisms by which alcohol may promote kidney dysfunction. One possible mechanism is oxidative stress resulting from increased production of reactive oxygen species, which leads to an excessive amount of free radicals, which in turn trigger tissue injury and increase inflammation. In addition, AUD's effect on other major organs (liver, heart, intestines, and skeletal muscle) appears to promote unfavorable pathological processes that are harmful to the kidneys. Notably, these mechanisms have not yet been validated experimentally in the kidney. Additional research is needed to clarify if alcohol does indeed promote kidney injury and the mechanisms by which alcohol-induced kidney injury may occur.

摘要

长期饮酒是众所周知的组织损伤风险因素。酒精使用障碍(AUD)与肾损伤之间的联系很有趣但存在争议,而且酒精可能损害肾脏的分子机制尚不清楚。迄今为止,试图将AUD与肾脏疾病联系起来的流行病学研究尚无定论,几乎没有实验证据直接将饮酒与肾损伤联系起来。然而,主要在其他器官和组织中进行的研究提出了几种酒精可能导致肾功能障碍的潜在机制。一种可能的机制是活性氧生成增加导致氧化应激,这会产生过量的自由基,进而引发组织损伤并加剧炎症。此外,AUD对其他主要器官(肝脏、心脏、肠道和骨骼肌)的影响似乎会促进对肾脏有害的不良病理过程。值得注意的是,这些机制尚未在肾脏中得到实验验证。需要更多的研究来阐明酒精是否确实会导致肾损伤以及酒精性肾损伤可能发生的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d032/5513691/51054d4630a4/arcr-38-2-283f1.jpg

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