-
Cureus Jul 2023Androgenic alopecia (AGA), commonly known as male pattern baldness (MPB), is a hereditary condition characterized by hair follicles that are sensitive to androgens. This... (Review)
Review
Androgenic alopecia (AGA), commonly known as male pattern baldness (MPB), is a hereditary condition characterized by hair follicles that are sensitive to androgens. This article focuses on examining the recent advancements in the comprehension and management of AGA. The genetic factors and pathophysiology of AGA, including the role of dihydrotestosterone (DHT) and the androgen receptor gene, are discussed. The consequences of hair loss on self-esteem and identity, as well as on mental health, are examined. Diagnostic methods, such as the hair-pull test and trichoscopy, are discussed. The article also presents the Hamilton-Norwood classification, which is the most commonly employed system for classifying MPB. The article then delves into the various treatment options available, including topical minoxidil, oral finasteride, platelet-rich plasma therapy, low-level light therapy, hair transplant, and other alternative treatments. The efficacy and combination therapies for these treatments are examined. Additionally, emerging treatments such as caffeine-based solutions and prostaglandin inhibitors are discussed. By examining the recent advancements in AGA treatment, this article provides a comprehensive overview for healthcare professionals to make informed decisions when selecting the best treatment options for their patients.
PubMed: 37663989
DOI: 10.7759/cureus.42768 -
The Journal of Urology Jan 2024Though the pathogenesis of benign prostatic hyperplasia is unclear, it was previously believed that increasing androgen levels contributed, though not all data support...
PURPOSE
Though the pathogenesis of benign prostatic hyperplasia is unclear, it was previously believed that increasing androgen levels contributed, though not all data support this idea. We tested if elevated serum testosterone or dihydrotestosterone were risk factors for lower urinary tract symptoms incidence in asymptomatic men and for lower urinary tract symptoms progression in symptomatic men.
MATERIALS AND METHODS
A post hoc analysis of REDUCE was performed in 3009 asymptomatic men and in 2145 symptomatic men. REDUCE was a randomized trial of dutasteride for prostate cancer prevention in men with an elevated prostate-specific antigen and negative prestudy biopsy. We estimated multivariable adjusted hazard ratios and 95% confidence intervals using Cox models to test the association between quintiles of serum testosterone and dihydrotestosterone at baseline and lower urinary tract symptoms incidence and progression and tested for interaction by treatment arm (dutasteride vs placebo).
RESULTS
In asymptomatic men, there was no evidence serum testosterone or dihydrotestosterone were related to lower urinary tract symptoms incidence ( = .9, = .4). In symptomatic men, there was no evidence serum testosterone or dihydrotestosterone were related to lower urinary tract symptoms progression ( = .9, = .7). Results were similar in both placebo and dutasteride arms (all interaction ≥ .3).
CONCLUSIONS
In REDUCE, higher serum testosterone and higher serum dihydrotestosterone were not associated with either lower urinary tract symptoms incidence in asymptomatic men or lower urinary tract symptoms progression in symptomatic men. These data do not support the hypothesis that serum androgens in middle-aged men are associated with lower urinary tract symptoms.
Topics: Humans; Male; Middle Aged; Dihydrotestosterone; Dutasteride; Incidence; Lower Urinary Tract Symptoms; Prostatic Hyperplasia; Testosterone; Randomized Controlled Trials as Topic
PubMed: 37873943
DOI: 10.1097/JU.0000000000003738 -
Journal of Advanced Research Mar 2024Apocynin (Apo), an NADPH oxidase (NOX) inhibitor, has been widely used to treat various inflammatory diseases. However, the therapeutic effects of Apo on benign...
INTRODUCTION
Apocynin (Apo), an NADPH oxidase (NOX) inhibitor, has been widely used to treat various inflammatory diseases. However, the therapeutic effects of Apo on benign prostatic hyperplasia (BPH), a multifactorial disease associated with chronic inflammation and hormone imbalance, remain unknown.
OBJECTIVES
The link between androgen signaling, reactive oxygen species (ROS), and prostate cell proliferation may contribute to the pathogenesis of BPH; therefore, the aim of this study was to identify the specific signaling pathway involved and to demonstrate whether the anti-oxidant Apo plays a role in the prevention and treatment of BPH.
METHODS
Ingenuity pathway analysis and si-RNA transfection were conducted to demonstrate the androgen receptor (AR) and NOX4 linkage in BPH. Pathological markers of BPH were measured by H&E staining, immunoblotting, ELISA, qRT-PCR, and immunofluorescence to examine the effect of Apo. Rats stimulated with testosterone and BPH-1 cells were used as BPH models.
RESULTS
AR and NOX4 network-mediated oxidative stress was upregulated in the BPH model. Next, we examined the effects of Apo on oxidative stress and chronic prostatic inflammation in BPH mouse models. In a testosterone-induced BPH rat model, Apo alleviated pathological prostate enlargement and suppressed androgen/AR signaling. Apo suppressed the upregulation of proinflammatory markers and promoted the expression of anti-oxidant factors. Furthermore, Apo regulated the TGF-β/Glut9/activin pathway and macrophage programming. In BPH-1 cells, Apo suppressed AR-mediated proliferation and upregulation of TGFB and NOX4 expression by alleviating oxidative stress. Apo activated anti-oxidant and anti-inflammatory systems and regulated macrophage polarization in BPH-1 cells. AR knockdown partially abolished the beneficial effects of Apo in prostate cells, indicating AR-dependent effects of Apo.
CONCLUSION
In contrast with existing BPH therapies, Apo may provide a new application for prostatic disease treatment, especially for BPH, by targeting the AR/TGF-β/NOX4 signaling pathway.
Topics: Mice; Male; Humans; Animals; Rats; Androgens; Receptors, Androgen; Antioxidants; Hyperplasia; Prostate; Prostatic Hyperplasia; Inflammation; Testosterone; Cell Proliferation; NADPH Oxidase 4; Acetophenones
PubMed: 37061215
DOI: 10.1016/j.jare.2023.04.006 -
Scientific Reports Oct 2023Penile size is closely concerned and short penis contributes serious sexual dysfunction and tremendous psychological problems to couples. Androgen is essential for...
Penile size is closely concerned and short penis contributes serious sexual dysfunction and tremendous psychological problems to couples. Androgen is essential for penile development and testosterone replacement is recommended to patients with micropenis. We previously proved that inhibiting activity of lysyl oxidase (Anti-lysyl oxidase, Anti-LOX) combined with vacuum erectile device (VED) lengthened penis by remodeling tunica albuginea. We thus explored whether HCG supplement could accelerate tunica albuginea remodeling (induced by Anti-LOX + VED) to promote penile growth. Forty-two SD male rats (4 weeks old) were purchased and divided into 7 groups: control, Anti-LOX, HCG, VED (with a negative aspirated pressure of - 300 mmHg), Anti-LOX + VED, HCG + VED, and Anti-LOX + HCG + VED. After an intervention for 4 weeks, all rats' penile length, exposed penile length, and erectile function were measured. Serum samples were collected to detect hormone levels and penile corpus cavernosum were harvested for histo-pathological analysis. All intervention groups showed significantly longer penis than controlled rats. Anti-LOX sharply increased penile length and exposed length by 15% and 9% respectively, this lengthening effect was more obvious in Anti-LOX + VED group (26% and 19%, respectively). Although HCG promoted penile length by 8%, this effect was slight for exposed length (3%). Moreover, Anti-LOX + HCG + VED dramatically increased penile length and exposed length by 22% and 18%, respectively, which was similar with that in Anti-LOX + VED (26% and 19%, respectively). HCG dramatically stimulated testosterone and dihydrotestosterone secretions than control group, whether with or without Anti-LOX and VED; while it induced more AR expression than other groups. Finally, all procedures did not improve or deteriorate normal erectile function. Although we verified that Anti-LOX + VED lengthened penis by inducing tunica albuginea remodeling, however, HCG supplement did not synergize with Anti-LOX + VED to accelerate albuginea remodeling to facilitate penile growth.
Topics: Humans; Male; Rats; Animals; Erectile Dysfunction; Penis; Penile Erection; Testosterone
PubMed: 37783699
DOI: 10.1038/s41598-023-38888-y -
Cancer Letters Jul 2023Castration-resistant prostate cancer (CRPC) responds poorly to existing therapy and appears as the lethal consequence of prostate cancer (PCa) progression. The tumour...
Castration-resistant prostate cancer (CRPC) responds poorly to existing therapy and appears as the lethal consequence of prostate cancer (PCa) progression. The tumour microenvironment (TME) has been thought to play a crucial role in CRPC progression. Here, we conducted single-cell RNA sequencing analysis on two CRPC and two hormone-sensitive prostate cancer (HSPC) samples to reveal potential leading roles in castration resistance. We described the single-cell transcriptional landscape of PCa. Higher cancer heterogeneity was explored in CRPC, with stronger cell cycling status and heavier copy number variant burden of luminal cells. Cancer-associated fibroblasts (CAFs), which are one of the most critical components of TME, demonstrated unique expression and cell-cell communication features in CRPC. A CAFs subtype with high expression of HSD17B2 in CRPC was identified with inflammatory features. HSD17B2 catalyses the conversion of testosterone and dihydrotestosterone to their less active forms, which was associated with steroid hormone metabolism in PCa tumour cells. However, the characteristics of HSD17B2 in PCa fibroblasts remained unknown. We found that HSD17B2 knockdown in CRPC-CAFs could inhibit migration, invasion, and castration resistance of PCa cells in vitro. Further study showed that HSD17B2 could regulate CAFs functions and promote PCa migration through the AR/ITGBL1 axis. Overall, our study revealed the important role of CAFs in the formation of CRPC. HSD17B2 in CAFs regulated AR activation and subsequent ITGBL1 secretion to promote the malignant behaviour of PCa cells. HSD17B2 in CAFs could serve as a promising therapeutic target for CRPC.
Topics: Male; Humans; Prostatic Neoplasms, Castration-Resistant; Cancer-Associated Fibroblasts; Sequence Analysis, RNA; Hormones; Cell Line, Tumor; Receptors, Androgen; Tumor Microenvironment; Estradiol Dehydrogenases; Integrin beta1
PubMed: 37244445
DOI: 10.1016/j.canlet.2023.216244 -
Redox Biology Sep 2023Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, has been used to treat several diseases. The present study aimed to investigate the therapeutic effects of...
Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, has been used to treat several diseases. The present study aimed to investigate the therapeutic effects of MitoQ in benign prostatic hyperplasia (BPH) models and their underlying molecular mechanisms. In this study, we determined that MitoQ inhibited dihydrotestosterone (DHT)-induced cell proliferation and mitochondrial ROS by inhibiting androgen receptor (AR) and NOD-like receptor family pyrin domain-containing 3 (NLRP3) signaling in prostate epithelial cells. Molecular modeling revealed that DHT may combine with AR and NLRP3, and that MitoQ inhibits both AR and NLRP3. AR and NLRP3 downregulation using siRNA showed the linkage among AR, NLRP3, and MitoQ. MitoQ administration alleviated pathological prostate enlargement and exerted anti-proliferative and antioxidant effects by suppressing the AR and NLRP3 signaling pathways in rats with BPH. Hence, our findings demonstrated that MitoQ is an inhibitor of NLPR3 and AR and a therapeutic agent for BPH treatment.
Topics: Male; Humans; Rats; Animals; Prostatic Hyperplasia; Antioxidants; Receptors, Androgen; NLR Family, Pyrin Domain-Containing 3 Protein
PubMed: 37454529
DOI: 10.1016/j.redox.2023.102816