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通过单细胞转录组分析探索糖尿病与勃起功能障碍之间的分子联系。

Exploring the Molecular Link Between Diabetes and Erectile Dysfunction Through Single-Cell Transcriptome Analysis.

作者信息

Begum Mahmuda, Choubey Mayank, Tirumalasetty Munichandra Babu, Arbee Shahida, Sadik Sibly, Mohib Mohammad Mohabbulla, Srivastava Shivani, Minhaz Naofel, Alam Riffat, Mohiuddin Mohammad Sarif

机构信息

Department of Internal Medicine, HCA-St. David's Medical Center, 919 E 32nd St, Austin, TX 78705, USA.

Department of Foundations of Medicine, NYU Grossman Long Island School of Medicine, 101 Mineola Blvd, Mineola, NY 11501, USA.

出版信息

Genes (Basel). 2024 Dec 13;15(12):1596. doi: 10.3390/genes15121596.

Abstract

Erectile dysfunction (ED) is a pathophysiological condition in which the patients cannot achieve an erection during sexual activity, and it is often overlooked yet prevalent among diabetic men, globally affecting approximately 35-75% of diabetic individuals. The precise mechanisms through which diabetes contributes to ED remain elusive, but the existing literature suggests the potential involvement of nerve and vascular damage that affects the penile supply. In the present review, we reanalyze the existing human single-cell transcriptomic data from patients having diabetes mellitus-associated ED with normal erections. The analysis validates the expression of genes associated with antioxidative pathways, growth factors, adipokines, angiogenesis, vascular functions, penile erection, sexual function, and inflammation in diverse cell types from healthy individuals and those with ED. Our transcriptomic analysis reveals alterations in the expression of adiponectin receptors in the pathogenesis of ED compared to their counterparts in healthy subjects. This comprehensive review sheds light on the molecular underpinnings of ED in the context of diabetes, providing an in-depth understanding of the biological and cellular alterations involved and paving the way for possible targeted therapeutic discoveries in the field of diabetes-associated male infertility.

摘要

勃起功能障碍(ED)是一种病理生理状况,患者在性活动期间无法勃起,它常常被忽视,但在糖尿病男性中很普遍,全球约35 - 75%的糖尿病患者受其影响。糖尿病导致ED的确切机制尚不清楚,但现有文献表明,神经和血管损伤可能参与其中,影响阴茎供血。在本综述中,我们重新分析了来自患有糖尿病相关ED但勃起功能正常患者的现有人类单细胞转录组数据。该分析验证了健康个体和ED患者不同细胞类型中与抗氧化途径、生长因子、脂肪因子、血管生成、血管功能、阴茎勃起、性功能和炎症相关基因的表达。我们的转录组分析揭示,与健康受试者相比,脂联素受体表达在ED发病机制中发生了改变。这一全面综述揭示了糖尿病背景下ED的分子基础,深入了解了其中涉及的生物学和细胞改变,并为糖尿病相关男性不育领域可能的靶向治疗发现铺平了道路。

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