Additionally, TBC1D20 regulates the formation of acrosomes via facilitating autophagy flux . Concretely, apical ES is localized at the contact surface between the Sertoli cell and the spermatids, and it is tightly connected to the sperm head via the acrosome, being an active participant in spermatozoa head shaping . Thus, energy imbalance, hyperthermia, and hypoxia all induce autophagy during spermatogenesis, while the inhibition of autophagy often relies on chemical inhibitors. Increased scrotal temperature generates testicular heat stress and induces testicular autophagy, later causing spermatogenic arrest . Additionally, amino acid supplementation is an efficient and effective strategy to increase spermatozoa quality, depending on the activation of autophagy .
The mammalian target of rapamycin (mTOR), a serine/threonine kinase, is a major regulator of cell growth, survival, metabolism, and immunity. Moreover, this review cannot fail to mention that endogenous estrogen signaling is essential for male reproduction . ABP is concentrated in the apical part of the SCs , promotes germ cell differentiation, and regulates spermatogenesis spatially . T, testosterone; ES, estradiol; NE, norepinephrine; NPY, neuropeptide; GABA, gamma-aminobutyric acid; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; FSH, follicle-stimulating hormone; KISS, kisspeptin; AVPV, anteroventral periventricular nucleus. Testosterone is mainly synthesized in LCs, where autophagy has been reported to be extremely active 54,97.
Classic macroautophagy is initiated from an isolated membrane (phagophore), which is followed by the formation of a double-membrane autophagosome that then delivers the engulfed proteins and fuses with lysosomes for degradation. Autophagy is a lysosomal degradation pathway that eliminates defective organelles and proteins from the cell. In humans, an alternative ABP transcript accumulates in germ cells in a highly regulated manner throughout the spermatogenic cycle3 and its expression is positively correlated with sperm motility4. ABP can also directly up-regulate the expression of aromatase in germ cells and oestrogen receptor beta2. ABP can promote germ cell differentiation and it has been reported that ABP up-regulates the expression of transition protein 1 (TP1), which is involved in nuclear chromatin condensation in rodent spermatids1. These data demonstrate that testosterone up-regulates ABP expression at least partially by suppressing the autophagic degradation.
The expression of LC3 was closely correlated with the accumulation of lipid droplets (LDs) as revealed by oil red O (ORO) staining (Fig. 1 E; Bilińska, 1994). Using a small-scale screen, a negative regulator of SR-BI, Na+/H+ exchanger regulatory factor 2 (NHERF2; gene name, Slc9a3r2), was found to be degraded via the autophagy–lysosome pathway. No use, distribution or reproduction is permitted which does not comply with these terms. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. Afzal A, Zhang Y, Afzal H, Saddozai UAK, Zhang L, Ji X-Y and Khawar MB (2024) Functional role of autophagy in testicular and ovarian steroidogenesis. By unraveling the complexities of this relationship, scientists and clinicians alike stand poised to revolutionize treatments for a myriad of endocrine disorders, ultimately enhancing reproductive health and quality of life.
Notably, the ER-resident chaperone Sig-1R, concentrated at MAMs, governs calcium dynamics and responses to oxidative stress (Gottschalk et al., 2022), suggesting its potential as a therapeutic target for conditions linked to ROS-induced damage in Leydig cells. Mitochondrial contact sites with the ER are vital for regulating ROS in gonadal cells. Notably, there may be additional connections between testosterone and autophagy. Concurrently, there is an increase in total cholesterol (TC) and LD levels in serum-free media. Stress reduces lipid droplets but increases testosterone release, effects counteracted by inhibiting autophagy.
It is possible that the induction of ABP by hypoxia is an adaptive response to hypoxia-induced cell death, maintaining a high concentration of ABP in the seminiferous tubule. However, in this study, we found that hypoxia-induced autophagy does not clear ABP. Therefore, it seems that the autophagic clearance of ABP is selectively regulated by testosterone. Clearance of ABP by autophagy can be enhanced or inhibited by rapamycin or CQ.
Moreover, we also observed similar effects of 3-MA and BafA1 on HsCG-induced autophagic flux in primary LCs in TM3 cells (Figure 2G-L). (A) Autophagy-related protein expression was analyzed by western blotting. These cells are usually chosen as a surrogate for primary LCs based on their sharing many properties of primary LCs . Here, we found a negative correlation of m6A modification with testosterone synthesis in LCs. It is noted that post-transcriptional modifications of eukaryotic mRNA play important roles in helping cells survive various stimuli . Cell growth and differentiation depend upon the fine-tuning regulation of gene expression at both transcriptional and translational levels . Previous studies have identified that AMP-activated protein kinase (AMPK), a major energy-sensing kinase, can promote autophagy to maintain energy homeostasis, whereas MTOR (mechanistic target of rapamycin kinase) can inhibit autophagy 14,15.

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