Neurobiological insights into lower urinary tract dysfunction: evaluating the role of brain-derived neurotrophic factor.

IF 1.5 Q3 UROLOGY & NEPHROLOGY
American journal of clinical and experimental urology Pub Date : 2023-12-15 eCollection Date: 2023-01-01
Chen Cheng, Qingfeng Li, Guiting Lin, Emmanuel C Opara, Yuanyuan Zhang
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Abstract

Lower urinary tract dysfunction (LUTD) encompasses a range of debilitating conditions that affect both sexes and different age groups. Understanding the underlying neurobiological mechanisms contributing to LUTD has emerged as a critical avenue for the development of targeted therapeutic strategies. Brain-derived neurotrophic factor (BDNF), a prominent member of the neurotrophin family, has attracted attention due to its multiple roles in neural development, plasticity, and maintenance. This review examines the intricate interplay between neurobiological factors and LUTD, focusing on the central involvement of BDNF. The review emphasizes the bidirectional relationship between LUTD and BDNF and explores how LUTD-induced neural changes may affect BDNF dynamics and vice versa. Growth factor therapy and the combined administration of controlled release growth factors and stem cells are minimally invasive treatment strategies for neuromuscular injury. Among the many growth factors and cytokines, brain-derived neurotrophic factor (BDNF) plays a prominent role in neuromuscular repair. As an essential neurotrophin, BDNF is involved in the modulation of neuromuscular regeneration through tropomyosin receptor kinase B (TrkB). Increasing BDNF levels facilitates the regeneration of the external urethral sphincter and contributes to the regulation of bladder contraction. Treatments targeting the BDNF pathway and sustained release of BDNF may become novel treatment options for urinary incontinence and other forms of lower urinary tract dysfunction. This review discusses the applications of BDNF and the theoretical basis for its use in the treatment of lower urinary tract dysfunction, including urinary incontinence (UI), overactive bladder (OAB), and benign prostatic hyperplasia (BPH), and in the clinical diagnosis of bladder dysfunction.

下尿路功能障碍的神经生物学启示:评估脑源性神经营养因子的作用。
下尿路功能障碍(LUTD)包括一系列使人衰弱的病症,对男女老少都有影响。了解导致下尿路功能障碍的潜在神经生物学机制已成为开发靶向治疗策略的重要途径。脑源性神经营养因子(BDNF)是神经营养素家族的重要成员,由于其在神经发育、可塑性和维持中的多重作用而备受关注。本综述探讨了神经生物学因素与 LUTD 之间错综复杂的相互作用,重点关注 BDNF 的核心参与作用。综述强调了 LUTD 和 BDNF 之间的双向关系,并探讨了 LUTD 引起的神经变化如何影响 BDNF 的动态,反之亦然。生长因子疗法以及控释生长因子和干细胞联合给药是神经肌肉损伤的微创治疗策略。在众多生长因子和细胞因子中,脑源性神经营养因子(BDNF)在神经肌肉修复中发挥着重要作用。作为一种重要的神经营养素,BDNF 通过肌球蛋白受体激酶 B(TrkB)参与神经肌肉再生的调节。提高 BDNF 水平可促进尿道外括约肌的再生,并有助于调节膀胱收缩。针对 BDNF 通路和 BDNF 持续释放的治疗方法可能成为尿失禁和其他形式下尿路功能障碍的新型治疗方案。本综述讨论了 BDNF 的应用及其在治疗尿失禁 (UI)、膀胱过度活动症 (OAB) 和良性前列腺增生症 (BPH) 等下尿路功能障碍以及膀胱功能障碍临床诊断中的理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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