Steroids最新文献

{"title":"Kumatakenin alleviates cadmium-induced testicular toxicity by restoring steroidogenesis and suppressing oxido-inflammatory responses.","authors":"Muhammad Umar Ijaz, Muhammad Zaid Salar, Moazama Batool, Shuonan Pang, Yubang Wang, Guoping Zhu","doi":"10.1016/j.steroids.2026.109856","DOIUrl":"https://doi.org/10.1016/j.steroids.2026.109856","url":null,"abstract":"<p><p>Cadmium (Cd) is a highly toxic compound that induces deleterious effects on living organisms and causes multi-organ toxicity, including testicular damage. Kumatakenin (KMK) is a flavonoid with potential antioxidant and anti-inflammatory properties. The present study was designed to assess the protective effects of KMK against Cd prompted testicular injury in rats. 24 albino rats were divided into four groups including control, Cd (5 mg/kg), Cd + KMK (5 mg/kg + 25 mg/kg) and KMK (25 mg/kg). Following a 56-day trial, the rats were anesthetized, dissected and further analyses were performed. The results showed that Cd caused significant oxidative damage in the testes via increasing ROS and MDA levels and lowering Nrf-2 & HO-1 mRNA expressions and antioxidant enzymes activities. Moreover, Cd increased the expressions of TLR4, MyD88, TRAF6 and NF-κB, which further increased the levels of inflammatory markers (TNF-α, COX-2, IL-1β & IL-6). Moreover, Cd exposure also resulted in significant upregulation in the mRNA expressions of pro-apoptotic markers (Bax and Caspase-3), while reducing the expressions of anti-apoptotic marker (Bcl-2) as well as steroidogenic markers (StAR, 3β-HSD, & 17β-HSD). Additionally, Cd lowered the levels of plasma testosterone which further caused a reduction in sperm count, and motility while increasing sperm abnormalities. Cd also induced histological disruptions in the testicular tissues. However, KMK treatment mitigated Cd induced disruptions in the testicular tissues. These outcomes demonstrate that KMK has the ability to modulate the mRNA expression of genes associated with the TLR4/NF-κB and Bax/Bcl-2/Caspase-3 pathways, thereby mitigating testicular injury.</p>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":" ","pages":"109856"},"PeriodicalIF":2.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “In silico analysis of Moringaceae derived potential drug-like compounds against Newcastle disease virus” [Steroids 219 (2025) 109628]","authors":"Muhammad Hammad Mustafa ,&nbsp;Fayyaz-ur Rehman ,&nbsp;Muhammad Ali ,&nbsp;Mohsin Javed ,&nbsp;Nazir Ahmad ,&nbsp;Tayyaba Shafique ,&nbsp;Ammar Zidan ,&nbsp;Ali Bahadur ,&nbsp;Shahid Iqbal ,&nbsp;Sajid Mahmood ,&nbsp;Abd-ElAziem Farouk ,&nbsp;Ibrahim Jafri","doi":"10.1016/j.steroids.2026.109750","DOIUrl":"10.1016/j.steroids.2026.109750","url":null,"abstract":"","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"228 ","pages":"Article 109750"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146107327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Donepezil enhances the testicular protective effect of metformin in diabetic rats by modulating steroidogenic signaling and Bax/Bcl-2/Caspase-3 pathway","authors":"Roland Eghoghosoa Akhigbe ,&nbsp;Joseph Chimezie ,&nbsp;Ajibola Ayomide Odeyemi ,&nbsp;Stella Olamide Oyesode ,&nbsp;Favour Adesogan ,&nbsp;Abimbola Ayoola Oladipo ,&nbsp;Precious Jesutofunmi Ashonibare ,&nbsp;Tunmise Maryanne Akhigbe ,&nbsp;Ebenezer Adeola Ashamu ,&nbsp;Michael A. Olamoyegun","doi":"10.1016/j.steroids.2026.109748","DOIUrl":"10.1016/j.steroids.2026.109748","url":null,"abstract":"<div><h3>Background</h3><div>Type 2 diabetes mellitus (T2DM) induces testicular damage through xanthine oxidase (XO)/uric acid (UA)/caspase-3-driven oxidative stress and apoptosis. Although metformin is effective in managing diabetes, combined therapy is more effective. Though donepezil protects against neuronal and retinal damage in diabetic rats, its role in diabetes-induced testicular damage is yet to be reported.</div></div><div><h3>Aim</h3><div>This study investigated the protective effects of combined metformin and donepezil treatment on testicular dysfunction in a high-fat diet/streptozotocin-induced T2DM rat model. Also, the involvement of XO/UA and Bax/Bcl-2/caspase signaling was examined.</div></div><div><h3>Methods</h3><div>Forty-eight 8-week-old male Wistar rats were randomly assigned into six equal groups: control, diabetes (DM), DM+metformin, donepezil, DM+donepezil, and DM+metformin+donepezil groups.</div></div><div><h3>Results</h3><div>T2DM caused testicular inflammation and oxidative stress, evidenced by elevated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), activation of NF-κB signaling, increased oxidative markers (MDA), and reduced antioxidant enzymes. T2DM also led to testicular apoptosis (increased Bax and caspase-3 and reduced Bcl-2). More so, T2DM repressed serum testosterone, FSH, and LH, and caused morphological disorganization of the testes, including germ cell loss and Leydig cell degeneration. Treatment with metformin and donepezil, singly or in combination, significantly mitigated these adverse effects, with the combined therapy demonstrating superior efficacy. The intervention suppressed XO/uric acid signaling, oxidative stress, and inflammatory responses via downregulation of NF-κB and apoptotic cascades. These results imply that donepezil and metformin work in concert to provide a potentially effective treatment strategy for reducing testicular damage caused by diabetes through modulation of oxidative, inflammatory, and apoptotic pathways, ultimately restoring testicular structure and function.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"228 ","pages":"Article 109748"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146057409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LCA and 3-oxo-LCA mitigate dietary oxysterols-induced loss of barrier function in intestinal epithelial cells","authors":"Gayatri Reghu ,&nbsp;Ashna Fathima ,&nbsp;Narendran Swaminathan ,&nbsp;Rajeev Sakhuja ,&nbsp;Trinath Jamma","doi":"10.1016/j.steroids.2026.109749","DOIUrl":"10.1016/j.steroids.2026.109749","url":null,"abstract":"<div><div>Loss of intestinal barrier integrity is a hallmark of many intestinal inflammations and associated diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). One of the primary factors contributing to intestinal epithelial barrier damage is a diet high in cholesterol. The non-enzymatically oxidized forms of dietary cholesterol, collectively known as oxysterols, have recently gained attention as mediators of various inflammatory conditions. In addition, oxysterols have been found to cause intestinal barrier damage via the loss of tight junction protein expression and promote inflammation. Secondary bile acids of host-gut microbial origin, and several other gut-microbiota-derived metabolites, are known to modulate intestinal inflammation. Here, we have studied the roles of two secondary bile acids in restoring barrier integrity and reducing the extent of dietary oxysterol-induced damage in intestinal epithelial cells. We found that oxysterols exert their damaging effects by inducing matrix metalloproteinases (MMP-2 and MMP-9) and activating NF-κB, which is coupled with the production of pro-inflammatory cytokines and chemokines (CCL2, CCL5, &amp; IL-8). Additionally, we also show that the secondary bile acids lithocholic acid (LCA) and dehydrolithocholic acid (3-oxo-LCA) counteract dietary oxysterol-induced loss of barrier function (TEER &amp; FITC-dextran flux). Overall, these findings provide supportive evidence for the potential role for secondary bile acids in maintaining barrier integrity and modulating inflammation in intestinal epithelial cells exposed to dietary oxysterols in vitro.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"228 ","pages":"Article 109749"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-acetyl-cysteine alleviates nandrolone decanoate-induced hippocampal cell apoptosis in rats via reversing protein expressions of S1P1, Akt and FOXO3a signaling pathway","authors":"Alireza Shirpoor ,&nbsp;Zahra Zarrini ,&nbsp;Roya Naderi","doi":"10.1016/j.steroids.2026.109759","DOIUrl":"10.1016/j.steroids.2026.109759","url":null,"abstract":"<div><div>Illicit use of nandrolone can result in apoptosis in the hippocampus tissue but the underlying mechanism is unknown. The present study evaluated the role of S1P1/Akt/FOXO3a pathway in hippocampus cell apoptosis following exposure to nandrolone decanoate either alone or in combination with <em>N</em>-acetyl-cysteine. Twenty-four male Wistar rats were randomly divided into three groups (n = 8): control, nandrolone (10 mg/kg; intramuscularly; three times per week), and nandrolone + <em>N</em>-acetyl-cysteine (150 mg/kg; intraperitoneally). After six weeks of treatment, the number of apoptotic cells was significantly increased in the nandrolone treated group compared with the control group. Compared to control group, nandrolone group showed significant upregulation of NOX2, iNOS, 8-OHdG, P-FOXO3a/FOXO3a and lactate dehydrogenase (LDH) protein expression in rat hippocampus cells. Conversely, the protein expressions of P-Akt/Akt and S1P1 were significantly downregulated in hippocampus tissue of rats treated with nandrolone compared with control rats. Co-administration of <em>N</em>-acetyl-cysteine with nandrolone significantly reduced the apoptotic index and reversed the expressions of S1P1, P-Akt/Akt and P-FOXO3a/FOXO3a in the hippocampus neurons compared with the nandrolone group. These findings suggest that S1P1/Akt/FOXO3a signaling pathway may at least in part play an important role in the progression of apoptosis induced by nandrolone exposure, providing new insights into the pathogenesis and potential treatment of nandrolone-induced hippocampal damage.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"228 ","pages":"Article 109759"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146081684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steroidal alkaloids: Exploring new therapeutic frontiers in cardiovascular diseases","authors":"Madhura Bapat,&nbsp;Kalyani Barve","doi":"10.1016/j.steroids.2026.109758","DOIUrl":"10.1016/j.steroids.2026.109758","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) still remain one of the leading causes of mortality worldwide, requiring novel therapeutic approaches. Steroidal alkaloids, a unique class of naturally bioactive compounds, have showcased promising pharmacological qualities in cardiovascular health. This review article explores the structural classification, pharmacokinetics, and pharmacodynamics properties of such alkaloids, emphasizing their potential therapeutic effects in CVDs. Key cardiovascular activities of these alkaloids include antihypertensive, vasodilatory, antiarrhythmic, and lipid-lowering effects, primarily mediated through receptor interactions, ion channel modulation, and enzyme inhibition. Clinical and preclinical research studies provide preliminary proof of efficacy, though significant research gaps still remain, including very clinical trials and incomplete mechanistic understanding. Furthermore, safety concerns regarding dose–response relationships, toxicity, and drug interactions must be addressed before clinical translation. Novel trends such as, targeted delivery systems, synthetic derivatives and multi-targeted approaches throw light upon the future potential of alkaloids in cardiovascular therapy. This review establishes the need for well-designed clinical trials and structure–activity relationship (SAR) studies to optimize these molecules for cardiovascular drug development. Further research studies integrating omics technologies and exploring the role of steroidal alkaloids in rare cardiovascular disorders could increase their therapeutic applicability.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"228 ","pages":"Article 109758"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective effects of luteolin and oleuropein against dexamethasone-induced hyperlipidemia","authors":"Lourin Nasr Aziz,&nbsp;Mohamed Omar Mahmoud,&nbsp;Ibrahim Taha Ibrahim","doi":"10.1016/j.steroids.2026.109746","DOIUrl":"10.1016/j.steroids.2026.109746","url":null,"abstract":"<div><h3>Background</h3><div>Dexamethasone-induced hyperlipidemia is a well-documented metabolic complication associated with prolonged glucocorticoid therapy. The present study aims to investigate the potential protective effects of the selected natural antioxidants luteolin and oleuropein against dexamethasone-induced hyperlipidemia.</div></div><div><h3>Methodology</h3><div>The study was conducted on five groups of female Wistar rats, including a normal control group, a dexamethasone-induced hyperlipidemia group, and three treatment groups. The treatment groups consisted of dexamethasone-administered rats receiving luteolin or oleuropein (100 mg/kg BW) individually or in combination (luteolin + oleuropein) for a duration of one month.</div></div><div><h3>Results</h3><div>Dexamethasone induced hyperlipidemia, hepatic injury, and oxidative stress, as evidenced by increased levels of aspartate aminotransferase (AST; +154%), alanine aminotransferase (ALT; +121%), total cholesterol (TC; +75%), triglycerides (+132%), and malondialdehyde (+85%), while reducing catalase and glutathione by approximately 50.5% and 62%, respectively, compared with the control group. Treatment with either luteolin or oleuropein individually mitigated these changes (AST: −47.0% and − 46.4%; ALT: −37.2% and − 36.4%; TC: −34.8% and − 33.1%; triglycerides: −41.7% and − 40.5%; malondialdehyde: −28.4% and − 26.0%; catalase: +79.2% and + 74.8%; and glutathione: +104.8% and + 102.3%, respectively). Combined treatment provided the greatest protection, and histological examination revealed partial restoration of normal hepatic architecture.</div></div><div><h3>Conclusion</h3><div>The study suggests that luteolin and oleuropein help counteract dexamethasone-induced hyperlipidemia. Their administration reduced oxidative stress and liver enzyme levels (AST, ALT, and ALP) and improved lipid profiles, indicating their potential as therapeutic agents against glucocorticoid-related metabolic disturbances. The enhanced effectiveness observed in the combined treatment groups likely reflects synergistic activity between these compounds<strong>.</strong></div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"227 ","pages":"Article 109746"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145947914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of multiple cardiotonic steroids in faecal material of untreated humans and rat strains","authors":"Zelie F. Masso ,&nbsp;Hannah Bint Ebrahim Mullah ,&nbsp;Anza Thiba ,&nbsp;Sarhana Dinat ,&nbsp;Ekene E. Nweke ,&nbsp;Gavin R. Norton ,&nbsp;Angela J. Woodiwiss ,&nbsp;A. Duncan Cromarty ,&nbsp;Geoffrey P. Candy","doi":"10.1016/j.steroids.2026.109747","DOIUrl":"10.1016/j.steroids.2026.109747","url":null,"abstract":"<div><div>Endogenous cardiotonic steroid (CTS) concentrations are raised in cardiovascular diseases. CTSs undergo gastro-hepatobiliary recirculation, with the gut being an important route of elimination, yet the presence of CTSs in faecal material is seldom reported. This study investigated methods to extract and identify the presence of CTSs in faecal material of rats and humans without prior treatment.</div></div><div><h3>Methods</h3><div>Freeze-dried faecal material from different untreated rat strains was extracted using various solvents, with separation and identification of CTSs using HPLC/MS. Preliminary results were obtained from human faecal material.</div></div><div><h3>Results</h3><div>Multiple CTSs were identified in faecal material, with marinobufagenin (MBG) predominant. Telocinobufagin was only detected in certain rat strains, whereas the extraction methods used did not recover ouabain. MBG and digoxin were elevated in Dahl salt sensitive rats fed supplementary salt. Bufalin was present in most spontaneously hypertensive rats (SHRs) but was not detectable in Wistar Kyoto rats (WKY). Conversely, digitoxin was detected in most WKYs but only few SHRs. Levels of digitoxin and bufalin remained relatively constant over 24 days in untreated rats. Solvent selection was critical in determining the CTSs extracted from human faecal material.</div></div><div><h3>Conclusions</h3><div>Multiple CTSs were detected in faecal material of untreated rats and humans. Steroids varied between rat strains and aligned with phenotype. Extraction requires further solvent optimisation and the use of tandem MS/MS is essential to reliably detect the profile of CTSs present. Analysis of CTSs present in readily available faecal material will enable studies to determine relationships between CTSs, the microbiome and disease progression.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"227 ","pages":"Article 109747"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145946411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"l-arginine mitigates endocrine and spermatogenesis disruptions in cisplatin-exposed male Wistar rats by modulating iNOS/NO/NF-kB and Nrf2/HO-1 signaling","authors":"O.O. Obembe ,&nbsp;G.A. Oyeniyi ,&nbsp;P.J. Ashonibare ,&nbsp;T.M. Akhigbe ,&nbsp;E.A. Ashamu ,&nbsp;R.E. Akhigbe","doi":"10.1016/j.steroids.2025.109738","DOIUrl":"10.1016/j.steroids.2025.109738","url":null,"abstract":"<div><h3>Background</h3><div>Even though cisplatin is highly effective in cancer treatment, its toxicity to non-target organs, such as the testes, remains a concern. Studies have shown that cisplatin induces testicular toxicity by activating an oxido-inflammatory response. Conversely, arginine exerts antioxidant and anti-inflammatory properties. Aim: Hence, the current study assessed the impact of arginine on cisplatin-induced testicular toxicity. In addition, the involvements of iNOS/NO/NF-kB and Nrf2/HO-1 signaling, which are key pathways in cisplatin toxicity, were probed. Materials and methods: Twenty-four male Wistar rats were acclimatized for two weeks and then randomized into 4 equal groups; control, arginine-treated, cisplatin-treated, and cisplatin + arginine-treated. Results: Arginine significantly attenuated cisplatin-induced reductions in sperm concentration, motility, and viability and increased the percentage of abnormal sperm morphology. More so, arginine markedly suppressed cisplatin-induced reductions in daily and total spermatid production, and circulating levels of GnRH, FSH, LH, and testosterone. Additionally, arginine improved cisplatin-induced distortion in testicular histology. These findings were associated with arginine-driven mitigation of cisplatin-induced rise in MDA, TNF-α, IL-6, IL-1β, iNOS, and NF-kB and cisplatin-induced decline in GSH, TAC, IL-10, NO, and Nrf2 levels and GR, SOD, catalase, and HO-1 activities. Conclusion: Summing up, arginine mitigated cisplatin-induced testicular endocrine and spermatogenesis disruption via the modulation of iNOS/NO/NF-kB and Nrf2/HO-1 signaling.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"226 ","pages":"Article 109738"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of reproductive steroids on autosomal dominant polycystic kidney disease progression in women","authors":"Noor Saeed Hasan,&nbsp;Warren Thomas","doi":"10.1016/j.steroids.2025.109726","DOIUrl":"10.1016/j.steroids.2025.109726","url":null,"abstract":"<div><div>Autosomal dominant polycystic kidney disease (ADPKD) is a disease characterized by the growth of fluid filled cysts in the kidney. ADPKD arises due to a heritable mutation in the polycystic kidney disease 1 gene (PKD1) and polycystic kidney disease 2 gene (PKD2) ultimately leading to kidney failure. Incidence in males and females is equivalent, but differences arise in progression. This review brings together various studies regarding the impact of cyclic hormone changes on ADPKD progression, bringing attention to gaps in knowledge that needs to be addressed. Circulating hormones play a crucial role in the pathogenesis of the disease, particularly the renin angiotensin system. The physiological actions of estrogen tend to have a protective effect on the kidney, contributing to a slowed progression in females. The hormonal changes of the menstrual cycle and at menopause result in changes in pathology via blood pressure fluctuation, promotion of renal repair and prevention of renal scarring and damage. Signaling pathways that are involved in cyst growth such as cAMP, mTOR, MAPK/ERK, and PI3K/Akt are modulated by estrogen, providing insights into potential mechanisms. Estrogen-based hormonal therapy is being investigated for its efficacy in improving renal function post menopause.</div></div>","PeriodicalId":21997,"journal":{"name":"Steroids","volume":"226 ","pages":"Article 109726"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145701625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}