Journal of Steroid Biochemistry and Molecular Biology最新文献

{"title":"Immobilization of cholesterol oxidases on functionalized Silica Nanoparticles for biotransformation of cholesterol and 7-ketocholesterol","authors":"Shubhrima Ghosh ,&nbsp;Razi Ahmad ,&nbsp;Vikas Kumar Gautam ,&nbsp;Sunil Kumar Khare","doi":"10.1016/j.jsbmb.2025.106774","DOIUrl":"10.1016/j.jsbmb.2025.106774","url":null,"abstract":"<div><div>Cholesterol oxidation leads to the development of several oxysterols such as 7-ketocholesterol (7KC), which are linked to various age-related conditions. An approach to reduce their toxicity is proposed using enzymes from microbial sources to degrade them. Our earlier studies identified <em>Pseudomonas aeruginosa</em> PseA and <em>Rhodococcus erythropolis</em> MTCC 3951 as potential strains capable of using 7KC as their sole carbon source. These strains produced cholesterol oxidase as the primary enzyme in the degradation pathway. To enhance applicability, cholesterol oxidase (ChOx) enzymes from <em>P. aeruginosa</em> PseA (ChOxP), <em>R. erythropolis</em> MTCC 3951 (ChOxR), and a commercial variant from <em>Streptomyces</em> sp. (ChOxS) were immobilized on silane functionalized silica nanoparticles (SNP) using covalent-coupling methods. The immobilization efficiency was 68 %, 86 %, and 83 % for ChOxP, ChOxR, and ChOxS respectively. The catalytic efficiency of the immobilized enzyme was nearly twice that of the free enzyme, with increased stability across a wide range of temperatures (10–70°C) and pH levels (4.0–9.0), although the optimum pH (7.5) and temperature (30°C) remained unchanged. The nano-immobilized cholesterol oxidases were reusable up to 10 cycles. Further, enzyme immobilization on nanoparticles was confirmed by FTIR, SEM, and TEM. Biotransformation of cholesterol and 7KC using the nanobioconjugates produced pharmaceutically important molecules 4-cholesten-3-one and 4-cholesten-3,7-dione respectively.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"252 ","pages":"Article 106774"},"PeriodicalIF":2.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144024266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"(-)-Epigallocatechin-3-gallate and chlorogenic acid in combination with vitamin D as a therapeutic approach for letrozole-induced polycystic ovary syndrome (PCOS) rats: Biochemical and hormonal modulation","authors":"Sana Siddiqui ,&nbsp;Rizwan Ahmad ,&nbsp;Tariq Aziz ,&nbsp;Aijaz Ahmed Khan ,&nbsp;Hamid Ashraf ,&nbsp;Shagufta Moin","doi":"10.1016/j.jsbmb.2025.106772","DOIUrl":"10.1016/j.jsbmb.2025.106772","url":null,"abstract":"<div><div>Treatment with phytochemicals have shown promising results in managing various diseases including Polycystic ovary syndrome (PCOS) which is an endocrine gynecological disorder affecting reproductive aged women. This study has demonstrated that Epigallocatechin-3-gallate (EGCG) and chlorogenic acid (CGA) in combination with vitamin D can significantly reduce PCOS like characteristics including ovarian cysts, hyperandrogenism, fasting blood glucose level, insulin resistance, hyperlipidaemia, ROS formation, oxidative stress, DNA damage, and ovarian histomorphology in letrozole induced PCOS rats. PCOS was induced in female Wistar rats by giving 1 mg/kg/day letrozole for 21 days through oral gavage. EGCG (100 mg/kg/day) and CGA (120 mg/kg/day) in combination with vitamin D (25 mcg/kg/day) was given orally for 15 days, from day 21–35. Metformin treatment was used as a positive control. Histological, microscopic analysis, and chemiluminescent immunoassays were performed to evaluate decrement in PCOS like symptoms. Nitric oxide (RNS) production, antioxidant status, and the generation of reactive oxygen species (ROS) were also assessed. Ovary homogenates and plasma samples of rats were also examined for markers of protein, lipid, and DNA oxidation. Activities of enzymatic antioxidants (superoxide dismutase, catalase, glutathione reductase, Paraoxonase-1 status) were also evaluated. EGCG + vitamin D and CGA + vitamin D has been found to restore hormonal balance by modulating steroidogenic enzymes, they also improved antioxidant enzyme activity including SOD, catalase, glutathione reductase, PON-1 arylesterase, PON-1 CMPAase, etc. Similarly, EGCG + vitamin D and CGA + vitamin D treatment have shown efficacy in normalizing the estrus cycle, reducing ovarian cysts, and improving ovarian histomorphology. They also assisted in alleviating triglycerides and cholesterol levels and maintained liver function enzymes level. However, EGCG + vitamin D proves to have better therapeutic potential modulates glucose metabolic pathways, by reducing blood glucose levels, advanced glycation end product formation, decreasing ROS generation and oxidative stress; consequently, lowers hyperandrogenism and insulin resistance. Overall, EGCG + vitamin D treatment offers a comprehensive approach in managing PCOS by targeting multiple pathways associated with this disorder, making it a potential alternative to conventional therapies.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"252 ","pages":"Article 106772"},"PeriodicalIF":2.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143929000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FSH, LH, lipid and adipokines in Polycystic Ovary Syndrome: Clinical biochemistry insights for diagnosis and management","authors":"Wafa Mansor Merza,&nbsp;Abeer Khalid Yaseen,&nbsp;Maha Adel Mahmood","doi":"10.1016/j.jsbmb.2025.106773","DOIUrl":"10.1016/j.jsbmb.2025.106773","url":null,"abstract":"<div><div>Polycystic Ovary Syndrome (PCOS) is a common endocrine syndrome characterized by hormonal imbalances, metabolic disturbances, and clinical symptoms. The pathophysiology of this syndrome involves disruptions in hormonal signaling, particularly changes in levels of luteinizing hormone (LH), and follicle-stimulating hormone (FSH) which can lead to anovulation and infertility. Additionally, insulin resistance and dysfunctional adipose tissue are other complicating factors of this condition. Biochemical markers such as FSH, LH, lipid profiles, and adipokines (like leptin and adiponectin) are crucial for diagnosing PCOS and assessing its severity. In PCOS patients, elevated LH levels relative to FSH are typically observed, and lipid abnormalities increase the risk of cardiovascular diseases. Diagnosing this syndrome usually requires comprehensive biochemical tests to confirm hyperandrogenism and insulin resistance. Management strategies include lifestyle modifications and pharmacological interventions aimed at correcting hormonal imbalances and dyslipidemia. Monitoring treatment outcomes through biochemical markers is essential for evaluating therapeutic efficacy. This review article examines the roles of FSH and LH hormones, lipids, and adipokines in the diagnosis and management of PCOS, emphasizing the importance of clinical biochemistry in improving diagnostic and treatment methods for this disorder. Furthermore, research into identifying emerging biomarkers for early diagnosis and new therapeutic targets is suggested.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"251 ","pages":"Article 106773"},"PeriodicalIF":2.7,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143912642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synthesis and preliminary evaluation of estradiol diselenocyanate derivatives as potential antitumor agents","authors":"Yanmin Huang,&nbsp;Yang Cheng,&nbsp;Wenhao Tian,&nbsp;Zhiping Liu,&nbsp;Chunfang Gan,&nbsp;Haifeng Chen,&nbsp;Tao Gan,&nbsp;Chunrui Cai,&nbsp;Jianguo Cui","doi":"10.1016/j.jsbmb.2025.106771","DOIUrl":"10.1016/j.jsbmb.2025.106771","url":null,"abstract":"<div><div>Cancer is a prominent disease that poses a significant threat to human health, and the exploration of highly efficient and low-toxicity anticancer drugs remains an active area of research. Leveraging the cell-penetrating and binding capabilities of steroids, along with the multifunctional pharmacological properties of selenocyano groups, novel compounds are being designed and synthesized with the aim of discovering highly efficient and minimally toxic anti-tumor drugs. In the present study, two selenocyano pharmacophores were incorporated into estradiol to synthesize a series of estradiol diselenocyanate derivatives with a 3-selenocyanoalkoxy-17-selenocyanoester structure. The results of antiproliferative activities evaluation demonstrated that the estradiol derivatives with 3-selenocyanobutoxy moiety exhibited potent inhibitory activity against tumor cell proliferation, especially for triple negative breast cancer cell line MDA-MB-231. Their antiproliferative efficacy was significantly superior to that of estradiol analogues with 3-selenocyanooctyloxy and corresponding monoselenocyanate precursors, indicating a synergistic effect upon introduction of the second selenocyano group on cytotoxicity. The <em>IC</em>₅₀ values for compound <strong>4g</strong> against HeLa, HepG-2, and MCF-7 cells were determined as 3.20, 3.17, and 5.41 μM respectively; notably lower than those observed for its corresponding monoselenocyano precursor <strong>3g</strong> which showed <em>IC</em>₅₀ values of 15.12, 16.09, and 9.44 μM, respectively. Remarkably, the <em>IC</em>₅₀ of compound <strong>4e</strong> against MDA-MB-231 cells is only 5.04 μM and exhibited significant inhibitory activity against MDA-MB-231 zebrafish xenograft tumors. The inhibition of these compounds on tumor cell proliferation was attributed to induction of apoptosis in these cells. Thus, the estradiol diselenocyanate compounds investigated herein hold great potential as novel antitumor drugs, and warrant further investigation.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"252 ","pages":"Article 106771"},"PeriodicalIF":2.7,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143924083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-coupled estrogen receptor reduces the breast cancer cell survival by regulating the IRE1α/miR-17-5p/TXNIP pathway","authors":"Maryam Mohammad-Sadeghipour ,&nbsp;Mohammad Hadi Nematollahi ,&nbsp;Maryam Sahebazzamani ,&nbsp;Hassan Ahmadinia ,&nbsp;Mohammad Reza Hajizadeh ,&nbsp;Mehdi Mahmoodi ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.jsbmb.2025.106770","DOIUrl":"10.1016/j.jsbmb.2025.106770","url":null,"abstract":"<div><div>This study aimed to explore whether GPER can induce the UPR response in the SKBR3 cell line through ER and IREα activation, and to assess whether this response leads to cell survival or cell death. Additionally, the study sought to evaluate the impact of this response on cell behaviors such as apoptosis, migration, and drug resistance. To activate the UPR and induce ER stress, we treated the MCF10A cell line with 0.5 µg/ml TUN for 24 and 48 h. The expression levels of XBP-1 and C/EBP homology protein (CHOP) genes (ER stress markers) were measured using the qRT-PCR technique. The MCF10A + TUN cell line was used as a positive control. To determine the optimal doses of G₁ and tamoxifen (TAM), we evaluated GPER expression using qRT-PCR analysis. Cells were then treated with various doses of G₁ (1000 nM), G₁₅ (1000 nM), and TAM (2000 nM), both individually and in combination (G₁ + G₁₅, TAM + G₁₅, G₁ + TAM), for 24 and 48 h. We measured the expression of GPER, IRE1α, MiR-17-5p, TXNIP, ABCB1, and ABCC1 genes. Apoptosis was assessed <em>via</em> flow cytometry, and cell migration was examined using the wound-healing assay. Our results demonstrated that GPER activation by G₁ and TAM significantly increased IRE1α expression in SKBR3 cells. This activation, through its RIDD activity, cleaved miR-17-5p and initiated the UPR death response. The upregulation of the TXNIP gene expression enhanced apoptosis and chemotherapy sensitivity while decreasing cell migration. Interestingly, these effects were notably reversed by G₁₅ treatment. In summary, the GPER/IRE1α/miR-17-5p/TXNIP axis plays a key role in the UPR pro-death response, promoting programmed cell death, reducing migration, and decreasing drug resistance in SKBR3 cells.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"252 ","pages":"Article 106770"},"PeriodicalIF":2.7,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143937144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steroid hormones in pain: Mechanistic underpinnings and therapeutic perspectives","authors":"Xinying Zhang ,&nbsp;Xiaolin Yang ,&nbsp;Yawei Ji ,&nbsp;Yidong Xu ,&nbsp;Yongjiu Ji ,&nbsp;Chenqi Jiang ,&nbsp;Suwan Hu ,&nbsp;Chun Yang","doi":"10.1016/j.jsbmb.2025.106769","DOIUrl":"10.1016/j.jsbmb.2025.106769","url":null,"abstract":"<div><div>Pain is a complex sensory and emotional experience that severely affects an individual's quality of life and health status. Steroid hormones, as important regulatory substances in the human body, are extensively involved in various physiological and pathological processes. In recent years, remarkable progress has been made in the research of steroid hormones in the field of pain. They play a crucial role in the occurrence, development, and treatment of pain. This review comprehensively elaborates on the roles and therapeutic mechanisms of steroid hormones in pain, explores the performances of glucocorticoids, mineralocorticoids, sex hormones, etc. in different pain models, as well as the molecular mechanisms by which they regulate pain through genomic and non-genomic effects, aiming to provide a theoretical basis for the clinical treatment of pain.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"251 ","pages":"Article 106769"},"PeriodicalIF":2.7,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of calcitriol on myeloid-derived suppressor cells in physiological aging","authors":"Yuliya V. Perfilyeva ,&nbsp;Aikyn Kali ,&nbsp;Diana S. Aben ,&nbsp;Yulduz R. Abdusattarova ,&nbsp;Anzhelika V. Lushova ,&nbsp;Yekaterina O. Ostapchuk ,&nbsp;Raikhan Tleulieva ,&nbsp;Anastassiya V. Perfilyeva ,&nbsp;Kamalidin O. Sharipov ,&nbsp;Timur I. Davlyatshin ,&nbsp;Nurshat Abdolla","doi":"10.1016/j.jsbmb.2025.106768","DOIUrl":"10.1016/j.jsbmb.2025.106768","url":null,"abstract":"<div><div>The active hormonal form of vitamin D, 1,25(OH)₂D, regulates many components of the immune system and previous research shows that 1,25(OH)₂D reduces the number and suppressive activity of MDSCs in tumors. This study aimed to evaluate the effects of calcitriol treatment on MDSCs in aged mice. We showed that aged BALB/c and CD1 mice exhibited increased levels of CD11b⁺Gr1⁺ cells in both the spleen and bone marrow compared to young mice. These cells displayed a less mature phenotype marked by reduced F4/80 expression and demonstrated robust T cell suppressive activity, as evidenced by their ability to inhibit the production of IFNγ and TNFα. Treatment of aged mice with calcitriol, administered twice weekly at a dose equivalent to 1 µg/kg for 4 weeks, significantly increased the population of CD11b⁺Gr1⁺ cells in the spleen, but not in the bone marrow of the animals, and promoted their differentiation into a more mature phenotype characterized by elevated F4/80 expression. In addition, calcitriol-treated aged mice exhibited significantly improved T cell responses, as indicated by increased IFNγ production upon specific antigen stimulation compared to the control group of mice. <em>In vitro</em>, calcitriol treatment of bone marrow-derived MDSCs similarly enhanced F4/80 expression without altering other markers such as CD11b, CD11c, or MHCII, and led to reduced expression of reactive oxygen species by these cells. Our study highlights the consistency of MDSC expansion across inbred and outbred mouse strains and supports the immunomodulatory role of calcitriol in promoting MDSC maturation and alleviating immune suppression in aging.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"251 ","pages":"Article 106768"},"PeriodicalIF":2.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NAT10 mediated polycystic ovary syndrome through the ac4C modification of CXCL14","authors":"Ding Wang,&nbsp;Hui Li,&nbsp;Qiaoling Wang,&nbsp;Yunxia Liu","doi":"10.1016/j.jsbmb.2025.106767","DOIUrl":"10.1016/j.jsbmb.2025.106767","url":null,"abstract":"<div><div>Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder among women of reproductive age, underscoring the critical importance of investigating its regulatory mechanisms. N-Acetyltransferase 10 (NAT10) is a crucial enzyme involved in mRNA acetylation modification, mediating target genes expression through N4-acetylcytidine (ac4C) modification to regulate the biological function of various diseases. Nonetheless, the specific role of NAT10 in PCOS regulation remains undisclosed. Ac4C dot hybridization experiment was conducted to determine ac4C expression in PCOS tissues. RT-qPCR was employed to assess the expression levels of NAT10 and CXCL14 in PCOS tissues and KGN cells. Cells viability was assessed using the CCK-8 method, while cell proliferation capacity was evaluated through the colony formation assay and EDU assay. Flow cytometry analysis was utilized to measure the apoptosis rate. The ac4C modification level was determined by acrp-qPCR analysis. RIP and luciferase reporter experiments confirmed the target binding relationship. The rat experiments confirmed the specific regulatory role of NAT10 in polycystic ovary syndrome in vivo. This study highlighted reduced levels of NAT10 and ac4C in PCOS, where silencing NAT10 boosts KGN cell proliferation and suppresses apoptosis. Additionally, NAT10-mediated ac4C modification governed the chemokine CXCL14 expression. Our research unveiled that NAT10 modulated PCOS occurrence and progression by enhancing the CXCL14 mRNA stability through acetylation, presenting potential novel insights into the mechanisms of mRNA acetylation in PCOS.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"251 ","pages":"Article 106767"},"PeriodicalIF":2.7,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of enzymes, neurosteroids, and synthetic steroids in neurodegenerative disorders: A critical review","authors":"Refik Servi ,&nbsp;Ramazan Fazıl Akkoç ,&nbsp;Feyza Aksu ,&nbsp;Süleyman Servi","doi":"10.1016/j.jsbmb.2025.106766","DOIUrl":"10.1016/j.jsbmb.2025.106766","url":null,"abstract":"&lt;div&gt;&lt;div&gt;Neurodegenerative disorders present a significant challenge to healthcare systems, mainly due to the limited availability of effective treatment options to halt or reverse disease progression. Endogenous steroids synthesized in the central nervous system, such as pregnenolone (PREG), dehydroepiandrosterone (DHEA), progesterone (PROG), and allopregnanolone (ALLO), have been identified as potential therapeutic agents for neurodegenerative diseases. Neurosteroids such as ALLO, DHEA, and PROG, as well as their synthetic analogs like Ganaxolene, Fluasterone, and Olexoxime, offer promising effects for conditions such as Alzheimer's disease (AD) and depression. Moreover, Brexanolone and Ganaxolone are synthetic steroids approved for the treatment of postpartum depression and epilepsy, respectively. Neurosteroids such as ALLO are crucial in modulating GABAergic neurotransmission and reducing neuroinflammation. These compounds enhance the activity of GABA-A receptors, leading to increased inhibitory signaling in the brain, which can help regulate mood, cognition, and neuroprotection. Small clinical trials and observational studies indicate that ALLO may have cognitive benefits, but no large-scale, definitive meta-analysis confirms a 20 % improvement in AD patients. Mitochondrial dysfunction plays a vital role in the pathogenesis of numerous neurological diseases due to the high-energy demand and sensitivity of neurons to oxidative stress. Reduced mitochondrial function leads to amyloid-beta plaques and tau tangles accumulation in AD. In Parkinson's disease (PD), mitochondrial dysfunction resulting from the PINK1 or Parkin genes leads to energy deficiencies and the accumulation of toxic byproducts. Mutations in genes such as SOD1, C9orf72, and TDP-43 have been associated with mitochondrial dysfunction in amyotrophic lateral sclerosis (ALS). Moreover, studies on these neurodegenerative diseases suggest that inflammation is not merely a consequence of neurodegeneration but is also an essential factor in this process. Many neurological disorders involve multifaceted interactions between genetics, the environment, and immune responses, making it difficult to pinpoint their exact causes. Future research aims to overcome these hurdles through genetic advances, regenerative medicine, and personalized therapies. Cutting-edge technologies such as artificial intelligence and high-throughput screening are expected to accelerate drug discovery and improve diagnostic accuracy. Increasing collaboration between interdisciplinary fields such as bioinformatics, neuroscience, and immunology will lead to innovative treatment strategies. This comprehensive review discusses the therapeutic effects of enzymes, neurosteroids, and synthetic steroids in different neurodegenerative diseases, particularly AD, PD, ALS, and MS. Potential challenges in the therapeutic use of neurosteroids, such as the limited bioavailability and off-target effects of synthetic steroids, are a","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"251 ","pages":"Article 106766"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143877103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low serum 25-hydroxy-vitamin D levels are associated with metabolic syndrome in a representative community population from Macau, China","authors":"Kaye E. Brock ,&nbsp;Elias Mpofu ,&nbsp;Shalinie King ,&nbsp;Rebecca S. Mason ,&nbsp;Michael J. Dibley ,&nbsp;Liang Ke","doi":"10.1016/j.jsbmb.2025.106765","DOIUrl":"10.1016/j.jsbmb.2025.106765","url":null,"abstract":"<div><div>Asians, especially Chinese have an increasingly high prevalence of vitamin D deficiency and insufficiency (serum 25-hydroxy-vitamin D 25(OH)D &lt; 30 nmol/L and &lt; 50 nmol/L, respectively). This population group also has a high prevalence of cardiometabolic risk factors such as Myocardial Infarction (MI), Metabolic Syndrome (MetS) and low blood levels of high-density lipoproteins (HDL) and high blood levels of triglycerides (TG). The aim of this analysis was to investigate these associations in a population from Macau, China. Blood, anthropometric, and physical data were collected from 1410 randomly selected residents of Macau. In this population, (55 % female, 19–89 years) 54 % were vitamin D insufficient. Results from categorical multivariate regression analyses (adjusted for age, sex, and physical activity, sitting and sunlight exposure) indicated significant two-fold associations between vitamin D insufficiency and prevalence of MI, MetS and low HDL and high TG levels. These associations became stronger when investigated with vitamin D deficiency (25(OH)D &lt; 30 nmol/L). The association between cardiometabolic factors and vitamin D deficiency in those older (≥60 yrs) increased markedly to OR MI= 9.48 (2.62–34.32), OR MetS= 7.82 (3.31–18.46) and OR low HDL= 8.68 (1.56–21.16) and OR high TG= 2.37 (1.07–5.25). These interesting observational findings suggest high vulnerability to lower 25(OH)D levels with related health disparities affecting older Asians. Integration of public health measures to detect vitamin D deficiency and insufficiency in Macau is important, and we suggest that routine health screening including serum 25(OH)D, HDL and TG in China may be protective for those at higher risk for related cardiometabolic conditions.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"252 ","pages":"Article 106765"},"PeriodicalIF":2.7,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}