Deletion of Sox30 in mice uniquely impairs testis development and spermatogenesis with complete absence of spermatozoa in testes leading to male infertility, but does not influence ovary development and female fertility.
Collectively, these results implicate that miR-509-5p may participate in the pathogenesis of male infertility and TGCT through regulating proliferation and apoptosis, two critical cellular activities for spermatogenesis and TGCT tumorigenesis.
In this review, we discuss the association of PCD genes and other axonemal genes with male infertility, drawing particular attention to possible differences between their functions in motile cilia and sperm tails.
In this review, we discuss the association of PCD genes and other axonemal genes with male infertility, drawing particular attention to possible differences between their functions in motile cilia and sperm tails.
In this review, we discuss the association of PCD genes and other axonemal genes with male infertility, drawing particular attention to possible differences between their functions in motile cilia and sperm tails.
In this review, we discuss the association of PCD genes and other axonemal genes with male infertility, drawing particular attention to possible differences between their functions in motile cilia and sperm tails.
Therefore, these data indicate that PRPS2 depletion contributes to the apoptosis of spermatogenic cells and is associated with hypospermatogenesis, which may be helpful for the diagnosis of male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
Fertility in men with hypospadias is impaired, as shown by lower birthrates, increased use of ART and higher risk of receiving a diagnosis of male infertility.
Fertility in men with hypospadias is impaired, as shown by lower birthrates, increased use of ART and higher risk of receiving a diagnosis of male infertility.
Our results uncover a previously unknown physiological role of NCOA5 in the regulation of epididymal sperm maturation and suggest that NCOA5 deficiency could cause male infertility through increased IL-6 expression in epididymis.
Our results uncover a previously unknown physiological role of NCOA5 in the regulation of epididymal sperm maturation and suggest that NCOA5 deficiency could cause male infertility through increased IL-6 expression in epididymis.