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高血压与糖尿病之间的相互影响:聚焦于妊娠及子代。一项系统综述。

Crosstalk between hypertension and diabetes: focusing on pregnancy and offspring. A systematic review.

作者信息

Alejandra Medina-Hernández, Ricardo Espinosa-Tanguma, Guadalupe Donjuán-Loredo

机构信息

Departamento de Fisiología y Biofísica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí, Mexico.

出版信息

Front Physiol. 2025 Apr 25;16:1519410. doi: 10.3389/fphys.2025.1519410. eCollection 2025.

DOI:10.3389/fphys.2025.1519410
PMID:40352144
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12061969/
Abstract

INTRODUCTION

The coexistence of diabetes mellitus (DM) and hypertension (HT) is very common; both pathologies seem to share different mechanisms such as insulin resistance (IR), endothelial dysfunction, increase in reactive oxygen species (ROS), among others. Furthermore, exposure to hyperglycemia during gestational development has been defined as a risk factor for cardiovascular disease (CVD) in adulthood. However, the mechanisms involved in this "prenatal programming" are still unclear. This review aims to identify the mechanisms involved in the relationship between DM and HT, both in their coexistence and in the development of HT in offspring derived from gestational diabetes (GD). There are no reviews that comprehensively cover both the link between HT and DM as well as the risk factors in mothers with GD and the cardiovascular effects in their offspring.

METHODS

A search of published studies reporting HT in offspring of diabetic pregnancies, either in animals or humans, prevalence and pathophysiological mechanisms of binomial hypertension-diabetes (HT/DM), mechanisms, metabolic alterations, DM and HT in pregnancy was done. Inclusion criteria were studies investigating the cardiovascular effects of GD on offspring, studies in animal models or humans, reviews and meta-analyses.

RESULTS

87 studies were included. IR is the main common factor between the presence of DM and the development of HT, in addition to inflammatory processes. Maternal pathology before pregnancy favors the development of diabetes and HT during pregnancy. Animal studies have shown that 100% of the offspring of mothers with GD have HT, mostly after 12 weeks of age. In human studies, there is a significant difference in the blood pressure (BP) levels of the offspring of mothers with gestational hyperglycemia compared with control mothers from the age of 2 years. Several mechanisms such as structural changes in the arterial wall, endoplasmic reticulum (RE) stress, increase in ROS and decrease in nitric oxide (NO) synthesis are proposed as some of the possible culprits.

CONCLUSION

Current evidence shows that the interaction between DM and HT occurs through mechanisms that they share in their pathogenesis, that is, the presence of one lead to the other and the hyperglycemia to which infants are exposed makes them more susceptible to CVD.

摘要

引言

糖尿病(DM)和高血压(HT)并存的情况非常常见;这两种病症似乎有不同的共同机制,如胰岛素抵抗(IR)、内皮功能障碍、活性氧(ROS)增加等。此外,孕期发育期间暴露于高血糖已被定义为成年后患心血管疾病(CVD)的一个风险因素。然而,这种“产前编程”所涉及的机制仍不清楚。本综述旨在确定DM和HT之间关系所涉及的机制,包括它们的并存情况以及妊娠期糖尿病(GD)后代中HT的发生发展机制。目前尚无综述全面涵盖HT与DM之间的联系、GD母亲的风险因素及其后代的心血管影响。

方法

检索已发表的关于糖尿病妊娠后代中HT的研究,包括动物或人类研究,以及二元高血压 - 糖尿病(HT/DM)的患病率和病理生理机制、机制、代谢改变、孕期的DM和HT。纳入标准为研究GD对后代心血管影响的研究、动物模型或人类研究、综述和荟萃分析。

结果

纳入了87项研究。除炎症过程外,IR是DM存在与HT发生之间的主要共同因素。孕前的母体病理状况有利于孕期糖尿病和HT的发展。动物研究表明,GD母亲的后代100%患有HT,大多在12周龄后。在人类研究中,与对照组母亲相比,妊娠期高血糖母亲的后代从2岁起血压(BP)水平存在显著差异。动脉壁结构变化、内质网(RE)应激、ROS增加和一氧化氮(NO)合成减少等几种机制被认为是一些可能的原因。

结论

目前的证据表明,DM和HT之间的相互作用是通过它们在发病机制中共享的机制发生的,即一种病症的存在会导致另一种病症,而婴儿所暴露的高血糖使他们更容易患CVD。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/0dd8cdcdb93f/fphys-16-1519410-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/719f389e45fe/fphys-16-1519410-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/7f071c3b082e/fphys-16-1519410-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/3b7f88483f48/fphys-16-1519410-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/0dd8cdcdb93f/fphys-16-1519410-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/719f389e45fe/fphys-16-1519410-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/7f071c3b082e/fphys-16-1519410-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/3b7f88483f48/fphys-16-1519410-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b8/12061969/0dd8cdcdb93f/fphys-16-1519410-g004.jpg

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Down-regulation of AMPK/PPARδ signalling promotes endoplasmic reticulum stress-induced endothelial dysfunction in adult rat offspring exposed to maternal diabetes.下调 AMPK/PPARδ 信号通路可促进母鼠糖尿病暴露致成年子代内皮细胞内质网应激诱导的内皮功能障碍。
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