Sperm mitochondria dysfunction in response to testicular cancer

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F23%3A00582890" target="_blank" >RIV/86652036:_____/23:00582890 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00064190:_____/23:10001075

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1111/eci.14146" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1111/eci.14146</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/eci.14146" target="_blank" >10.1111/eci.14146</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Sperm mitochondria dysfunction in response to testicular cancer

Popis výsledku v původním jazyce

Testicular cancer is the most common form of cancer in young men of reproductive age and its incidence is increasing globally. With the currently successful treatment and 95% survival rate, there is a need for deeper understanding of testicular cancer-related infertility. Most patients with testicular cancer experience semen abnormalities prior to cancer therapy. However, the exact mechanism of the effect of testicular cancer on sperm anomalies is not known. Mitochondria are organelles that play a crucial role in both tumorigenesis and spermatogenesis and their malfunction may be an important factor resulting in sperm abnormalities in testicular cancer patients. Within the scope of this review, we will discuss current knowledge of testicular cancer-related alterations in the ATP production pathway, a possible pathophysiological switch from oxidative phosphorylation (OXPHOS) to glycolysis, as well as the role of oxidative stress promoting sperm dysfunction. In this regard, the review provides a summary of the impact of testicular cancer on sperm quality as a possible consequence of impaired mitochondrial function including the energy metabolic pathways that are known to be altered in the sperm of testicular cancer patients.

Název v anglickém jazyce

Sperm mitochondria dysfunction in response to testicular cancer

Popis výsledku anglicky

Testicular cancer is the most common form of cancer in young men of reproductive age and its incidence is increasing globally. With the currently successful treatment and 95% survival rate, there is a need for deeper understanding of testicular cancer-related infertility. Most patients with testicular cancer experience semen abnormalities prior to cancer therapy. However, the exact mechanism of the effect of testicular cancer on sperm anomalies is not known. Mitochondria are organelles that play a crucial role in both tumorigenesis and spermatogenesis and their malfunction may be an important factor resulting in sperm abnormalities in testicular cancer patients. Within the scope of this review, we will discuss current knowledge of testicular cancer-related alterations in the ATP production pathway, a possible pathophysiological switch from oxidative phosphorylation (OXPHOS) to glycolysis, as well as the role of oxidative stress promoting sperm dysfunction. In this regard, the review provides a summary of the impact of testicular cancer on sperm quality as a possible consequence of impaired mitochondrial function including the energy metabolic pathways that are known to be altered in the sperm of testicular cancer patients.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30218 - General and internal medicine

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

European Journal of Clinical Investigation

ISSN

0014-2972

e-ISSN

1365-2362

Svazek periodika

DEC 2023

Číslo periodika v rámci svazku

2023-12-17

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

—

Kód UT WoS článku

001116965300001

EID výsledku v databázi Scopus

2-s2.0-85178963674