English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

animals and human beings. According to these results, overexpression of hKLK1 might counteract the effect of ROCK system and prevent the inevitable age-related fibrosis of the penis. Although the study showed a possible new target of the treatment of ED, the conclusions arising from this experiment are difficult to interpret. In our opinion, the conclusions of this study could have been affected by several limitations. First, we think that the evaluation of penile fibrosis, which represents the main endpoint of this study, may be not adequate. The authors performed a semiquantitative method, Masson’s trichrome, for the evaluation of collagen content in the penis. In our opinion, a quantitative method like Western blot analysis for collagen and elastin content of the corpora cavernosa could be more accurate.10,11 Second, the author stated in the conclusion that the fibrosis prevention is due to the inhibition of the ROCK pathway without investigating the effect of the hKLK1 on the NO system. NO represents the main actor of the penile erection mechanism and, additionally, it is well known for its antifibrotic properties.1,5 More important, data suggest that effectors of the activated NO pathway may inhibit the ROCK pathway. Under this point of view, the activation of NO system may be responsible for the protective effects of hKLK. This aspect represents, in our opinion, the main limit of the study, especially because the same group had already shown, in a recently very similar study, that hKLK1 could play a preventive role in age-related erectile dysfunction by activation of the NO-cGMP pathway and inhibition of the RhoA-ROCK pathway.12 Despite its limitations, this study adds valuable data to the literature suggesting that hKLK gene therapy can benefit patients with age-related ED by attenuating the penile fibrotic process. The question of how the activation of kallikrein system is able to prevent the age-related penile fibrosis needs to be addressed.

Kallikrein-kinin system: is it the fountain of youth?