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Peer-reviewedCC BYCurrent sexual health reports

Mechanistic Insights on Immune Activation-Driven Erectile Dysfunction: Evidence from Animal Models.

  • Tiago T Gonçalves1,2,3
  • Raiana Dos Anjos Moraes1,2,3
  • Rinaldo Rodrigues Dos Passos1,2,3
  • Clinton Webb1,2,3
  • Fernanda Priviero1,2,3
  1. 1Cardiovascular Translational Research Center, Floyd School of Medicine, University of South Carolina, Columbia, SC 29208, USA.
  2. 2Department of Biomedical Engineering, Molinaroli College of Engineering and Computing, University of South Carolina, Columbia, SC, USA.
  3. 3Department of Cell Biology and Anatomy, Floyd School of Medicine, University of South Carolina, Columbia, SC, USA.
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Abstract

Purpose of review

Erectile dysfunction (ED) has traditionally been attributed to impaired hemodynamics and reduced nitric oxide (NO) bioavailability. This review examines current evidence supporting immune activation and inflammation as shared mechanisms contributing to ED across diverse pathological conditions.Recent findings

Experimental studies demonstrate that diabetes, hypertension, obesity, aging, nerve injury, and psychological stress are associated with activation of inflammatory pathways including NF-κB, Toll-like receptors, and the NLRP3 inflammasome. These pathways interact with oxidative stress and endothelial dysfunction to promote cytokine production, fibrosis, smooth muscle loss, and inflammatory cell death.Summary

Current evidence identifies inflammatory and innate immune pathways as convergent pathogenic drivers of ED across diverse etiologies. Rather than representing passive consequences of underlying disease, these mechanisms actively contribute to vascular, neural, and structural dysfunction, perpetuating processes that promote erectile impairment. Recognizing the central role of immune-mediated dysfunction in ED may facilitate the development of novel therapeutic strategies targeting disease mechanisms rather than symptoms alone.

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Cite

BibTeXRIS
BibTeX
@article{goncalves2026mechanistic,
  title = {{Mechanistic Insights on Immune Activation-Driven Erectile Dysfunction: Evidence from Animal Models.}},
  author = {Tiago T Gonçalves and Raiana Dos Anjos Moraes and Rinaldo Rodrigues Dos Passos and Clinton Webb and Fernanda Priviero},
  journal = {Current sexual health reports},
  year = {2026},
  month = aug,
  doi = {10.1007/s11930-026-00426-y},
  url = {https://europepmc.org/article/MED/42903725},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Mechanistic Insights on Immune Activation-Driven Erectile Dysfunction: Evidence from Animal Models.
AU  - Tiago T Gonçalves
AU  - Raiana Dos Anjos Moraes
AU  - Rinaldo Rodrigues Dos Passos
AU  - Clinton Webb
AU  - Fernanda Priviero
PY  - 2026
DA  - 2026/08/26
JO  - Current sexual health reports
DO  - 10.1007/s11930-026-00426-y
UR  - https://europepmc.org/article/MED/42903725
AB  - Purpose of review  Erectile dysfunction (ED) has traditionally been attributed to impaired hemodynamics and reduced nitric oxide (NO) bioavailability. This review examines current evidence supporting immune activation and inflammation as shared mechanisms contributing to ED across diverse pathological conditions.Recent findings  Experimental studies demonstrate that diabetes, hypertension, obesity, aging, nerve injury, and psychological stress are associated with activation of inflammatory pathways including NF-κB, Toll-like receptors, and the NLRP3 inflammasome. These pathways interact with oxidative stress and endothelial dysfunction to promote cytokine production, fibrosis, smooth muscle loss, and inflammatory cell death.Summary  Current evidence identifies inflammatory and innate immune pathways as convergent pathogenic drivers of ED across diverse etiologies. Rather than representing passive consequences of underlying disease, these mechanisms actively contribute to vascular, neural, and structural dysfunction, perpetuating processes that promote erectile impairment. Recognizing the central role of immune-mediated dysfunction in ED may facilitate the development of novel therapeutic strategies targeting disease mechanisms rather than symptoms alone.
SN  - 1548-3584
SN  - 1548-3592
ER  -