Результаты исследований: Научные публикации в периодических изданиях › Обзорная статья › Рецензирование
Pathogenesis of autoimmune male infertility : Juxtacrine, paracrine, and endocrine dysregulation. / Chereshnev, Valeriy A.; Pichugova, Svetlana V.; Beikin, Yakov B.; Chereshneva, Margarita V.; Iukhta, Angelina I.; Stroev, Yuri I.; Churilov, Leonid P.
в: Pathophysiology, Том 28, № 4, 12.2021, стр. 471-488.Результаты исследований: Научные публикации в периодических изданиях › Обзорная статья › Рецензирование
}
TY - JOUR
T1 - Pathogenesis of autoimmune male infertility
T2 - Juxtacrine, paracrine, and endocrine dysregulation
AU - Chereshnev, Valeriy A.
AU - Pichugova, Svetlana V.
AU - Beikin, Yakov B.
AU - Chereshneva, Margarita V.
AU - Iukhta, Angelina I.
AU - Stroev, Yuri I.
AU - Churilov, Leonid P.
N1 - Chereshnev, V.A.; Pichugova, S.V.; Beikin, Y.B.; Chereshneva, M.V.; Iukhta, A.I.; Stroev, Y.I.; Churilov, L.P. Pathogenesis of Autoimmune Male Infertility: Juxtacrine, Paracrine, and Endocrine Dysregulation. Pathophysiology 2021, 28, 471-488. https://doi.org/10.3390/pathophysiology28040030
PY - 2021/12
Y1 - 2021/12
N2 - According to global data, there is a male reproductive potential decrease. Pathogenesis of male infertility is often associated with autoimmunity towards sperm antigens essential for fertil-ization. Antisperm autoantibodies (ASAs) have immobilizing and cytotoxic properties, impairing spermatogenesis, causing sperm agglutination, altering spermatozoa motility and acrosomal reaction, and thus preventing ovum fertilization. Infertility diagnosis requires a mandatory check for the ASAs. The concept of the blood–testis barrier is currently re-formulated, with an emphasis on informational paracrine and juxtacrine effects, rather than simple anatomical separation. The etiology of male infertility includes both autoimmune and non-autoimmune diseases but equally develops through autoimmune links of pathogenesis. Varicocele commonly leads to infertility due to testicular ischemic damage, venous stasis, local hyperthermia, and hypoandrogenism. However, varicocelectomy can alter the blood–testis barrier, facilitating ASAs production as well. There are contradictory data on the role of ASAs in the pathogenesis of varicocele-related infertility. Infection and inflammation both promote ASAs production due to “danger concept” mechanisms and because of antigen mimicry. Systemic pro-autoimmune influences like hyperprolactinemia, hypoandrogenism, and hypothyroidism also facilitate ASAs production. The diagnostic value of various ASAs has not yet been clearly attributed, and their cut-levels have not been determined in sera nor in ejaculate. The assessment of the autoimmunity role in the pathogenesis of male infertility is ambiguous, so the purpose of this review is to show the effects of ASAs on the pathogenesis of male infertility.
AB - According to global data, there is a male reproductive potential decrease. Pathogenesis of male infertility is often associated with autoimmunity towards sperm antigens essential for fertil-ization. Antisperm autoantibodies (ASAs) have immobilizing and cytotoxic properties, impairing spermatogenesis, causing sperm agglutination, altering spermatozoa motility and acrosomal reaction, and thus preventing ovum fertilization. Infertility diagnosis requires a mandatory check for the ASAs. The concept of the blood–testis barrier is currently re-formulated, with an emphasis on informational paracrine and juxtacrine effects, rather than simple anatomical separation. The etiology of male infertility includes both autoimmune and non-autoimmune diseases but equally develops through autoimmune links of pathogenesis. Varicocele commonly leads to infertility due to testicular ischemic damage, venous stasis, local hyperthermia, and hypoandrogenism. However, varicocelectomy can alter the blood–testis barrier, facilitating ASAs production as well. There are contradictory data on the role of ASAs in the pathogenesis of varicocele-related infertility. Infection and inflammation both promote ASAs production due to “danger concept” mechanisms and because of antigen mimicry. Systemic pro-autoimmune influences like hyperprolactinemia, hypoandrogenism, and hypothyroidism also facilitate ASAs production. The diagnostic value of various ASAs has not yet been clearly attributed, and their cut-levels have not been determined in sera nor in ejaculate. The assessment of the autoimmunity role in the pathogenesis of male infertility is ambiguous, so the purpose of this review is to show the effects of ASAs on the pathogenesis of male infertility.
KW - Antisperm autoantibodies
KW - Autoimmune thyroiditis
KW - Ejaculate
KW - Male infertility
KW - Orchitis
KW - Sperm antigens
KW - Spermatozoa
KW - Varicocele
KW - Varicocelectomy
UR - http://www.scopus.com/inward/record.url?scp=85117930409&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/9f54a865-3500-327c-a2f5-b81a04068017/
U2 - 10.3390/pathophysiology28040030
DO - 10.3390/pathophysiology28040030
M3 - Review article
AN - SCOPUS:85117930409
VL - 28
SP - 471
EP - 488
JO - Pathophysiology
JF - Pathophysiology
SN - 0928-4680
IS - 4
ER -
ID: 88126920