Is It Possible to Regenerate the Underactive Detrusor? Part 1. Molecular and Stem Cell Therapies Targeting the Urinary Bladder and Neural Axis - ICI-RS 2024.

IF 1.8 3区 医学 Q3 UROLOGY & NEPHROLOGY
Neurourology and Urodynamics Pub Date : 2025-03-01 Epub Date: 2024-10-07 DOI:10.1002/nau.25597
Sanjay Sinha, Francisco Cruz, Esther Martinez Cuenca, Mikolaj Przydacz, George Bou Kheir, Anthony J Kanai, Andries Van Huele, Jerzy B Gajewski, Tufan Tarcan, Jason M Lazar, Jeffrey P Weiss, Pradeep Tyagi, Paul Abrams, Alan Wein
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引用次数: 0

Abstract

Introduction: Detrusor muscle weakness is commonly noted on urodynamics in patients with refractory voiding difficulty. No approved therapies have been proven to augment the strength of a detrusor voiding contraction.

Methods: This subject was discussed by a think-tank at the International Consultation on Incontinence- Research Society (ICI-RS) meeting held in Bristol, June 2024. The discussions of the think-tank are being published in two parts. This first part discusses molecular and stem cell therapies targeting the urinary bladder and the neural axis.

Results: Senescence of the urothelium and extracellular ATP acting through P2X3 receptors might be important in detrusor underactivity. Several molecules such as parasympathomimetics, acotiamide, ASP8302, neurokinin-2 agonists have been explored but none has shown unequivocal clinical benefit. Different stem cell therapy approaches have been used, chiefly in neurogenic dysfunction, with some studies showing benefit. Molecular targets for the neural axis have included TRPV-4, Bombesin, and serotoninergic receptors and TAC-302 which induces neurite growth.

Conclusions: Several options are currently being pursued in the search for an elusive molecular or stem cell option for enhancing the power of the detrusor muscle. These encompass a wide range of approaches that target each aspect of the contraction mechanism including the urothelium of bladder and urethra, myocyte, and neural pathways. While none of these have shown unequivocal clinical utility, some appear promising. Lessons from other fields of medicine might prove instructive.

Clinical trial registration: Not necessary. Not a clinical trial.

有可能使功能不全的逼尿肌再生吗?第 1 部分 针对膀胱和神经轴的分子和干细胞疗法 ICI-RS 2024。
导言:难治性排尿困难患者在尿动力学检查中通常会发现逼尿肌无力。目前还没有任何已获批准的疗法可增强逼尿肌排尿收缩的强度:方法:2024 年 6 月在布里斯托尔举行的尿失禁国际咨询研究会(ICI-RS)会议上,智囊团讨论了这一主题。智囊团的讨论将分两部分发表。第一部分讨论针对膀胱和神经轴的分子和干细胞疗法:结果:尿路神经细胞的衰老和通过P2X3受体发挥作用的细胞外ATP可能是导致逼尿肌活动不足的重要原因。目前已探索了多种分子,如拟副交感神经药物、阿可替胺、ASP8302、神经激肽-2激动剂等,但均未显示出明确的临床疗效。已采用不同的干细胞治疗方法,主要用于神经源性功能障碍,一些研究显示了其益处。神经轴的分子靶点包括TRPV-4、蚕豆素、5-羟色胺能受体和诱导神经元生长的TAC-302:结论:在寻找难以捉摸的分子或干细胞方案以增强逼尿肌力量的过程中,目前有几种方案正在进行中。这些方法范围广泛,针对收缩机制的各个方面,包括膀胱和尿道的尿路上皮细胞、肌细胞和神经通路。虽然这些方法都没有显示出明确的临床效用,但其中一些似乎很有前景。临床试验注册:临床试验注册:不必要。不是临床试验。
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来源期刊
Neurourology and Urodynamics
Neurourology and Urodynamics 医学-泌尿学与肾脏学
CiteScore
4.30
自引率
10.00%
发文量
231
审稿时长
4-8 weeks
期刊介绍: Neurourology and Urodynamics welcomes original scientific contributions from all parts of the world on topics related to urinary tract function, urinary and fecal continence and pelvic floor function.
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