Mechanisms of angiotensin II to induce depression in diabetes.

IF 1.2 Q4 ENDOCRINOLOGY & METABOLISM
Diabetology International Pub Date : 2025-04-05 eCollection Date: 2025-07-01 DOI:10.1007/s13340-025-00817-x
Renata Vargas, Adriana Pedreañez, Yenddy Carrero, Juan P Hernandez-Fonseca, Hugo Hernandez-Fonseca, Jesús A Mosquera
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引用次数: 0

Abstract

The expression of angiotensin II (Ang II) has been reported in diabetes associated with hypertension and inflammatory processes. It has also been reported a link between Ang II, depression and diabetes; however, underlying mechanisms of Ang II-induced depression in this disease remain unclear. This review focuses on the possible mechanisms of Ang II to induce depression in diabetes. Ang II can induce pro-inflammatory events that activate indoleamine 2,3-dioxygenase and kynurenine monooxygenase. These activated enzymes act by decreasing the production of serotonin and increasing the production of quinolinic acid which acts on the N-methyl-d-aspartate receptor and the amino-methyl propionic acid receptor inducing decreased brain-derived neurotrophic factor (BDNF) expression and depression. Ang II can also induce the production of galectin 3 which has a depressant effect. Neuroinflammation induced by Ang II during diabetes can alter brain cells, event associated with functional disorders and depression. Furthermore, Ang II is capable of inducing oxidative stress in diabetes linked to depressive behaviors. In conclusion, Ang II has the potential to induce depression during diabetes through different mechanisms that involve inflammatory processes, oxidative stress, the production of galectin 3, and decrease in serotonin and BDNF. These findings open the possibility of using anti-Ang II drugs for the treatment of depressive behavior in diabetes.

血管紧张素II诱导糖尿病患者抑郁的机制。
血管紧张素II (Ang II)的表达在高血压和炎症过程相关的糖尿病中有报道。也有报道称Ang II、抑郁症和糖尿病之间存在联系;然而,这种疾病中Ang ii诱导抑郁的潜在机制尚不清楚。本文就Ang II诱导糖尿病患者抑郁的可能机制进行综述。Ang II可以诱导激活吲哚胺2,3-双加氧酶和犬尿氨酸单加氧酶的促炎事件。这些激活的酶通过减少血清素的产生和增加喹啉酸的产生来起作用,喹啉酸作用于n-甲基-d-天冬氨酸受体和氨基-甲基丙酸受体,诱导脑源性神经营养因子(BDNF)表达减少和抑郁。Angⅱ还能诱导凝集素3的产生,具有抑制作用。糖尿病患者由angii引起的神经炎症可改变脑细胞,发生与功能障碍和抑郁相关的事件。此外,Ang II能够在与抑郁行为相关的糖尿病中诱导氧化应激。总之,Ang II有可能通过不同的机制诱导糖尿病患者的抑郁,包括炎症过程、氧化应激、凝集素3的产生、血清素和BDNF的降低。这些发现开启了使用抗angii药物治疗糖尿病抑郁行为的可能性。
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来源期刊
Diabetology International
Diabetology International ENDOCRINOLOGY & METABOLISM-
CiteScore
3.90
自引率
4.50%
发文量
42
期刊介绍: Diabetology International, the official journal of the Japan Diabetes Society, publishes original research articles about experimental research and clinical studies in diabetes and related areas. The journal also presents editorials, reviews, commentaries, reports of expert committees, and case reports on any aspect of diabetes. Diabetology International welcomes submissions from researchers, clinicians, and health professionals throughout the world who are interested in research, treatment, and care of patients with diabetes. All manuscripts are peer-reviewed to assure that high-quality information in the field of diabetes is made available to readers. Manuscripts are reviewed with due respect for the author''s confidentiality. At the same time, reviewers also have rights to confidentiality, which are respected by the editors. The journal follows a single-blind review procedure, where the reviewers are aware of the names and affiliations of the authors, but the reviewer reports provided to authors are anonymous. Single-blind peer review is the traditional model of peer review that many reviewers are comfortable with, and it facilitates a dispassionate critique of a manuscript.
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