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Purpose <p>Lower urinary tract symptoms (LUTS) can result from several conditions, including but not limited to benign prostatic hyperplasia, diabetes, stress urinary incontinence, and metabolic syndrome. In 2011, it was estimated that nearly 2 billion people (45.2% of the world population) experience one or more LUTS. To date, there is no single underlying mechanism identified in lower urinary tract symptoms or the associated conditions. However, a recent body of evidence has demonstrated that mitochondrial dysfunction may contribute to conditions associated with LUTS. Furthermore, patients with inherited mitochondrial disease exhibit lower urinary tract symptoms at rates above the general population. Given that mitochondrial dysfunction is an under-investigated area of urinary disease research, this review aims to summarize the existing literature in the field.</p> Methods <p>PubMed was used as the primary database for literature search. Keywords included “lower urinary tract symptoms”, “mitochondria”, “urinary dysfunction”; additionally, once identified, further disease-specific searches were performed (e.g., “urinary dysfunction in type 1 diabetes”). Studies published earlier than August 2025 were included, and a specific focus was placed on clinical or human studies. Urologic conditions lacking at least three publications investigating mitochondrial dysfunction were not included; studies examining mitochondrial dysfunction in urologic cancers were also outside the scope of this review.</p> Results and conclusions <p>Mitochondrial dysfunction is a potential novel intersection of diseases associated with LUTS, including aging, metabolic syndrome, diabetes, stress urinary incontinence, benign prostatic hyperplasia, and overactive bladder. While initial studies are promising, more investment into identifying underlying mechanisms and new potential treatments is needed. Additionally, as mitochondrial modulators undergo trial as treatments in other conditions, careful consideration should be given to their potential as treatments for LUTS.</p> <p></p>

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Mitochondrial dysfunction in urologic disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月24日

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  • Alexis E. Adrian,
  • Natalie J. Boucher,
  • Kevin T. McVary,
  • Donald B. DeFranco,
  • William A. Ricke

摘要

Purpose

Lower urinary tract symptoms (LUTS) can result from several conditions, including but not limited to benign prostatic hyperplasia, diabetes, stress urinary incontinence, and metabolic syndrome. In 2011, it was estimated that nearly 2 billion people (45.2% of the world population) experience one or more LUTS. To date, there is no single underlying mechanism identified in lower urinary tract symptoms or the associated conditions. However, a recent body of evidence has demonstrated that mitochondrial dysfunction may contribute to conditions associated with LUTS. Furthermore, patients with inherited mitochondrial disease exhibit lower urinary tract symptoms at rates above the general population. Given that mitochondrial dysfunction is an under-investigated area of urinary disease research, this review aims to summarize the existing literature in the field.

Methods

PubMed was used as the primary database for literature search. Keywords included “lower urinary tract symptoms”, “mitochondria”, “urinary dysfunction”; additionally, once identified, further disease-specific searches were performed (e.g., “urinary dysfunction in type 1 diabetes”). Studies published earlier than August 2025 were included, and a specific focus was placed on clinical or human studies. Urologic conditions lacking at least three publications investigating mitochondrial dysfunction were not included; studies examining mitochondrial dysfunction in urologic cancers were also outside the scope of this review.

Results and conclusions

Mitochondrial dysfunction is a potential novel intersection of diseases associated with LUTS, including aging, metabolic syndrome, diabetes, stress urinary incontinence, benign prostatic hyperplasia, and overactive bladder. While initial studies are promising, more investment into identifying underlying mechanisms and new potential treatments is needed. Additionally, as mitochondrial modulators undergo trial as treatments in other conditions, careful consideration should be given to their potential as treatments for LUTS.