Hepatocyte Growth Factor (HGF) expression in high-fat diet fed rat corpus cavernosum. Preliminary results

I. Tomada*, N. Tomada, F. Marques, P. Vendeira, D. Neves

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)


The main cause of erectile dysfunction (ED) is organic in nature, with vasculogenic etiology being predominant. Several epidemiological studies report the relationship between ED and several well-recognized cardiovascular risk factors, including atherosclerosis, diabetes, dyslipidemia, hypertension, as well as lifestyle factors, such as obesity and sedentarism. Recent findings also indicate that high-fat (HF) regular intake induces endothelial dysfunction and increases ED prevalence. Due to their interconnection, ED is considered equivalent to endothelial dysfunction, and it is nowadays seen as a predictive factor of atherosclerosis and cardiovascular disease (CVD). It is well established that the expression of some vascular growth factors is frequently diminished in corpus cavernosum (CC) of ED patients, and that its levels are particularly modified in metabolic syndrome (MetS). This syndrome combines more than three of the illnesses that prompt to vasculogenic ED: elevated blood pressure, high triglycerides, low high-density lipoprotein (HDL) cholesterol, elevated waist circumference, and insulin resistance. Hepatocyte Growth Factor (HGF) is a pleiotropic factor with potent mitogenic and angiogenic properties, previously employed in the treatment of ischaemic members. Interestingly, it was demonstrated that its serum levels were particularly increased in obesity and in MetS. HGF is expressed by several organs, but as far as we know, it has never been detected in CC. In this way, we present an immunohistochemical (IH) characterization of HGF expression in HF-diet fed rat CC.
Original languageEnglish
Pages (from-to)126-129
Number of pages4
JournalMicroscopy and Microanalysis
Issue numberSUPPL. 3
Publication statusPublished - Sept 2008
Externally publishedYes


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