ArticleSexual medicine2024
Identification of fibrosis-related genes and biomarkers in diabetic erectile dysfunction.
Article in Sexual medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- From symptomatic relief to restorative medicine: a comprehensive review of diabetic erectile dysfunction.Translational andrology and urology · 2026Review
- Erectile Dysfunction in Diabetes Mellitus: A Comprehensive Narrative Review of Pathophysiology, Genetic Association Studies and Therapeutic Approaches.Endocrinology, diabetes & metabolism · 2025Review
- Current status and advances in adipose-derived stem cells therapy for diabetes mellitus erectile dysfunction.Frontiers in medicine · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Diabetic erectile dysfunction (DMED) has a high incidence and is poorly treated. Aim: This study investigates fibrosis's genetic profiling and explores potential mechanisms for DMED. Methods: The DMED model was constructed in rats using streptozotocin. Erectile function was quantified using cavernous nerve electrostimulation. Fibrosis was evaluated using Masson's staining. RNA-seq was employed to analyze differentially expressed genes and fibrosis-related genes (FRGs) were acquired. Function enrichment analyses were performed, and genetic interaction was analyzed. Hub FRGs were screened using machine learning algorithms and Cytoscape tools and validated in Gene Expression Omnibus databases. Moreover, biological roles and subpopulation distribution of hub FRGs were determined. Outcomes: Fibrosis-related genetic functions may play a vital role in DMED. Results: Based on comprehensive analysis, 45 differentially expressed FRGs were identified. These genes participate in regulating smooth muscle cell proliferation, vasoconstriction, and collagen-associated activities. Final analyses identified and validated a core gene signature comprising TIMP1, BMP7, and POSTN. They were closely associated with diabetic complications-related signaling pathways and extracellular matrix-receptor interaction. Clinical Translation: The identified fibrosis-related gene signature may serve as the novel biomarkers for treating DMED. Strengths and Limitations: The study is the first to investigate the genetic profiles behind fibrosis and DMED using comprehensive approaches. However, the validation is not adequate and more animal experiments are needed. Conclusion: The gene profiling and biological functions of FRGs in DMED were identified. These results broaden the understanding of fibrosis in DMED.
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