Several recent studies have suggested a link between AAA proteases-dependent mitochondrial protein quality control and muscle quality/function maintenance. While modulating mitochondrial gene expression through testosterone in skeletal muscle holds promise for enhancing muscle health, performance, and metabolism, it also presents risks and complexities that require careful control and examination. Testosterone's effects on mitochondrial gene expression could potentially help to improve metabolic health by enhancing mitochondrial function and energy metabolism in skeletal muscle, thereby reducing the risk of metabolic diseases. Specifically, our aim was to investigate whether testosterone exerts a direct regulatory influence on the expression of mitochondrial genes involved in maintaining mitochondrial integrity and functionality, thus contributing to the aforementioned preservation and protection of these organelles. These results strongly suggest that testosterone indirectly regulates mitochondrial gene expression in the skeletal muscle, probably via the activation of the NRF/TFAM-TFBM/mitochondrial genes axis.
This enzyme converts cholesterol into pregnenolone, the first building block in the chain of reactions that leads to testosterone. Once cholesterol is inside the mitochondria, it undergoes a chemical transformation. This is made possible by a special protein called StAR (Steroidogenic Acute Regulatory protein). Pregnenolone is then converted into other hormones, eventually resulting in testosterone. It begins with cholesterol, a type of fat molecule, being transported into the mitochondria.
Pharmaceuticals targeting mitochondrial function, termed 'mitoceuticals' (Yonutas et al., 2020), are rapidly becoming the future of translational mitochondrial research. This group asserts that aromatase activity and interactions between testosterone metabolites with both the androgen and estrogen receptor play a major role in the behavioral and mitochondrial deficits seen in this disorder (Celec et al., 2015; Frye et al., 2008). The role of hormones and mitochondrial dysfunction in the development of anxiety is robust, with hormonal changes and mitochondrial dysfunction seen in both human and rodent models (Shimamoto and Rappeneau, 2017). Together, these data suggest a major role of estrogen signaling and ERß in mitochondrial regulation in the development of AD. The influence in sex steroid hormones and AD development reveals a strong connection between hormone concentration, mitochondrial function, and behavioral changes. This suggests pinpointed alteration in mitochondrial dysfunction giving rise to the specific, learning and memory related deficits of the disease. Both mitochondrial function and transport are hindered by tau and Aß, with evidence of a fourfold reduction in mitochondria within the presynaptic terminals in Broadman's area 41 and 42, areas heavily targeted by AD neurodegeneration (Pickett et al., 2018).
These findings suggest that testosterone production amplifies the transfer of intercellular materials from LCs to tMacs. This treatment markedly reduced the levels of serum LH and testosterone in adult Cyp17a1Cre; R26tdTomato mice (Supplementary Fig. 1a–c). To validate these observations in vivo, we treated Cyp17a1Cre; R26tdTomato mice with hCG to induce an increase in serum testosterone levels (Fig. 1e,f).
Here we identify a mitochondrial transfer network between LCs and different testicular macrophage (tMac) subpopulations. Despite these challenges, LCs exhibit remarkable longevity and minimal turnover, suggesting the existence of specialized mechanisms that maintain LC mitochondrial homeostasis under such constrains. As an undergraduate at the College of William and Mary, Ms. Shaw investigated the interaction between cell-cycle control and embryonic neural development of Xenopus laevis.
Scale bars, 2 μm (left) and 200 nm (right; magnified views of the boxed regions). Scale bars, 5 μm (confocal image) and 0.5 μm (magnified 3D reconstructions of the boxed regions). Following isolation from Cx3cr1GFP mice using FACS, tMac-EVs were subjected to proteomics analysis. Scale bars, 5 μm (main image) and 0.5 μm (inset, 3D reconstruction of the boxed regions). B, Experimental strategy to label tMacs with GFP and membrane-targeted tdTomato in Cx3cr1GFP; mTmG mice. Super-resolution fluorescence microscopy analysis demonstrated that membrane-surrounded tMac-derived particles were released extracellularly (Fig. 5c).

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