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逼尿肌活动低下与衰老和代谢综合征的关系:来自动物模型的提示。

Association of detrusor underactivity with aging and metabolic syndrome: suggestions from animal models.

机构信息

Department of Physiology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku-shi, Kochi 783-8505, Japan.

出版信息

J Smooth Muscle Res. 2024;60:23-30. doi: 10.1540/jsmr.60.23.

DOI:10.1540/jsmr.60.23
PMID:39085088
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11291108/
Abstract

Detrusor underactivity, a condition in which the bladder muscle does not contract strongly or long enough to empty the bladder completely or within the normal time frame, is a common cause of lower urinary tract symptoms in older individuals of both sexes. Although aging is a known risk factor for detrusor underactivity, its pathophysiological mechanisms are not fully understood. Therefore, establishing animal models that closely mimic the pathophysiology of detrusor underactivity in humans is necessary to elucidate these mechanisms. Metabolic syndrome is a cluster of several risk factors, including obesity, hyperlipidemia, hyperglycemia, and hypertension, which are associated with the development of diabetes, cardiovascular disease, and lower urinary tract dysfunction in both sexes. Notably, bladder dysfunction resulting from detrusor underactivity is observed at an earlier age in animal models with diabetes mellitus than in those without. Recently, detrusor underactivity-like phenotypes have been observed at a relatively early age in animal models with metabolic syndrome, involving obesity, hyperlipidemia, and hypertension, compared with those without. Therefore, this review introduces the association of detrusor underactivity with aging and metabolic syndrome, as well as possible pathophysiological mechanisms for detrusor underactivity from reports of various animal models. Notably, metabolic syndrome may accelerate the onset of age-related detrusor underactivity, and further analysis of old animal models with metabolic syndrome may help elucidate the pathogenesis of detrusor underactivity in humans.

摘要

逼尿肌活动低下,即膀胱肌肉收缩无力或时间不够长,无法完全排空膀胱或在正常时间内排空,是老年男女下尿路症状的常见原因。虽然衰老已知是逼尿肌活动低下的一个危险因素,但其病理生理机制尚未完全阐明。因此,建立能够密切模拟人类逼尿肌活动低下病理生理学的动物模型对于阐明这些机制是必要的。代谢综合征是一组多种危险因素的集合,包括肥胖、高血脂、高血糖和高血压,这些因素与糖尿病、心血管疾病和两性下尿路功能障碍的发展有关。值得注意的是,与没有糖尿病的动物模型相比,糖尿病动物模型中逼尿肌活动低下导致的膀胱功能障碍在更早的年龄就出现了。最近,与没有代谢综合征的动物模型相比,肥胖、高血脂和高血压等代谢综合征相关因素的动物模型在相对较早的年龄就出现了逼尿肌活动低下样表型。因此,本综述介绍了逼尿肌活动低下与衰老和代谢综合征的关联,以及从各种动物模型报告中推测出的逼尿肌活动低下的可能病理生理机制。值得注意的是,代谢综合征可能会加速与年龄相关的逼尿肌活动低下的发生,对具有代谢综合征的老年动物模型进行进一步分析可能有助于阐明人类逼尿肌活动低下的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/11291108/07fe70dc576a/jsmr-60-023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/11291108/21a4e90a3ea4/jsmr-60-023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/11291108/07fe70dc576a/jsmr-60-023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/11291108/21a4e90a3ea4/jsmr-60-023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/11291108/07fe70dc576a/jsmr-60-023-g002.jpg

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本文引用的文献

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Hypertens Res. 2024 Apr;47(4):987-997. doi: 10.1038/s41440-024-01597-8. Epub 2024 Feb 14.
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Underactive Bladder and Detrusor Underactivity: New Advances and Prospectives.膀胱过度活动症和逼尿肌活动低下:新进展与展望。
Int J Mol Sci. 2023 Oct 24;24(21):15517. doi: 10.3390/ijms242115517.
3
Detrusor underactivity is associated with metabolic syndrome in aged primates.
逼尿肌活动低下与老年灵长类动物的代谢综合征有关。
Sci Rep. 2023 Apr 25;13(1):6716. doi: 10.1038/s41598-023-33112-3.
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Overview and New Insights into the Metabolic Syndrome: Risk Factors and Emerging Variables in the Development of Type 2 Diabetes and Cerebrocardiovascular Disease.代谢综合征概述及新认识:2 型糖尿病和心脑血管疾病发展中的危险因素和新兴变量。
Medicina (Kaunas). 2023 Mar 13;59(3):561. doi: 10.3390/medicina59030561.
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Inflammation triggered by the NLRP3 inflammasome is a critical driver of diabetic bladder dysfunction.由NLRP3炎性小体引发的炎症是糖尿病膀胱功能障碍的关键驱动因素。
Front Physiol. 2022 Nov 25;13:920487. doi: 10.3389/fphys.2022.920487. eCollection 2022.
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Metabolic Syndrome and Overactive Bladder Syndrome May Share Common Pathophysiologies.代谢综合征与膀胱过度活动症可能具有共同的病理生理学机制。
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