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Volume 18, Issue 2 (March 2016) 18, 282–291; DOI:10.4103/1008-682X.170445
Proteomic signatures of infertile men with clinical varicocele and their validation studies reveal mitochondrial dysfunction leading to infertility
Ashok Agarwal, Rakesh Sharma, Luna Samanta, Damayanthi Durairajanayagam, Edmund Sabanegh
1American Center for Reproductive Medicine, Cleveland Clinic, Cleveland, OH, USA; 2Department of Zoology, School of Life Sciences, Ravenshaw University,
Cuttack ‑ 751 003, Odisha, India; 3Faculty of Medicine, MARA University of Technology (UiTM), Selangor, Darul Ehsan, Malaysia; 4Department of Urology, Cleveland
Clinic, Cleveland, OH, USA.
Correspondence: Prof. A Agarwal (agarwaa@ccf.org)
| Abstract |
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INTRODUCTION
Varicocele is diagnosed in about 15%–20% of the adult male population
and is implicated as a factor in about 40% of infertile men.1 The
recommendation of the American Society of Reproductive Medicine is to
treat a varicocele when it is palpable and present with at least one abnormal
semen parameter in couples presenting with infertility or when the female
partner is normal.2 Numerous factors have been proposed to explain the
occurrence of this multifactorial disease, which include venous stasis,
testicular hypothermia, testicular hypoxia, apoptosis, heavy metal toxicity,
increased oxidative stress, and increased DNA damage.3,4 Although poor
semen quality, increased oxidative stress and DNA fragmentation are
frequently observed, not all men presenting with varicocele are infertile,
and men with high‑grade varicocele can still father children.5–7 However,
the underlying molecular mechanism of varicocele‑associated testicular
dysfunction and infertility remains unclear.
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