Smoking, Genetic Susceptibility and Early Menopause: Unveiling Biological Mechanisms and Potential Therapy Targets DOI
Yuhang Liang, Jie Ou,

Jing Fu

et al.

BJOG An International Journal of Obstetrics & Gynaecology, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 27, 2024

ABSTRACT Objective To explore the association between smoking, genetic susceptibility and early menopause (EM) clarify potential mechanisms underlying this relationship. Design An observational Transcriptome‐wide analysis (TWAS) study. Setting UK Biobank public summary statistics. Population 139 869 women with full baseline data, no gynaecological surgery history. Methods Adjusted modified Poisson regression models were developed to determine smoking risk effects on EM. TWAS was used identify gene expression EM, Mendelian randomisation (MR) infer causality. Enrichment explored regulatory networks of transcription factors, microRNAs therapeutic targets. Small molecule drugs predicted using drug‐gene interaction analysis. Main Outcome Measures EM prevalence common patterns. Results Women over 30 pack‐years had about 1.5 times higher risk, RRs 1.39 (95%CI, 1.23–1.56), 1.45 (1.33–1.59) (1.36–1.55) in low, intermediate high groups. identified hub genes such as IMMP2L, BMPR2 HMGN1. MR confirmed daily cigarette consumption a causal factor menopause. Several targets (e.g., SP600125, INCB18424 ruxolitinib) identified. Conclusions Smoking reduction significantly lowered Hub provided new avenues for mitigating harmful smoking.

Language: Английский

Targeted inhibition of ferroptosis in bone marrow mesenchymal stem cells by engineered exosomes alleviates bone loss in smoking-related osteoporosis DOI Creative Commons
Yao Wang, Lin Sun, Zixu Dong

et al.

Materials Today Bio, Journal Year: 2025, Volume and Issue: unknown, P. 101501 - 101501

Published: Jan. 1, 2025

Smoking-related osteoporosis (SROP) is characterized by reduced bone mass, primarily due to the accumulation of tobacco-derived toxins. This study demonstrates activation ferroptosis and reactive oxygen species (ROS)-related pathways in marrow mesenchymal stem cells (BMSCs) SROP mice. Here, we integrated genetic engineering bone-targeting peptide modification develop innovative engineered exosomes. Using techniques, introduced α-1,3-fucosyltransferase 6 (Fut6), a key protein involved prostate cancer metastasis, identified exosomes expressing Fut6 (F6-exo) with capabilities. Additionally, modified these peptide, (AspSerSer)6, synthesize F6-(DSS)6-exo. F6-(DSS)6-exo enabled targeted delivery curcumin, restoring osteogenic differentiation potential BMSCs mitigating loss mouse models. In summary, this highlights combination hydrophobic diacylglycerol insertion as novel therapeutic approach for SROP.

Language: Английский

Citations

0
Causal association among smoking, bitter beverage consumption, and risk of osteoporosis: a two-sample mendelian randomization-based study DOI Creative Commons
Yanqian Wu, J. Chao, Min Bao

et al.

Hereditas, Journal Year: 2025, Volume and Issue: 162(1)

Published: Jan. 24, 2025

Abstract Objectives Two-sample MR methods were employed to analyze the impact of smoking and bitter beverage consumption on risk osteoporosis with pathological fractures, in order assess causal association. Methods Publicly available genome-wide association study summary data analyzed using methods. The exposures investigated (smoking per day, initiation, lifetime index) beverages (coffee, tea, alcoholic beverages, non-alcoholic total beverages). outcomes examined fractures. inverse-variance weighted (IVW) method was used as main statistical model. stability reliability results verified by Cochran’s Q test, Egger-intercept leave-one-out analysis. Results Smoking day causally associated OR = 1.417, 95% CI 1.119–1.794, P 0.003), index had a possible genetic fractures (OR 4.187, 1.909–9.184, < 0.001). No found between initiation or ( > 0.05). identified Total showed potential effect 3.687, 1.535–8.858, 0.003 3.040, 1.466–6.304, 0.002, respectively). Conclusions This raises based genetics. Certain are linked an increased risk.

Language: Английский

Citations

0
Associations between smoking and osteoporosis and all-cause mortality in participants from the United States: a cohort study DOI Creative Commons

Xiaoqin Qu,

Jie-Xian Jiang,

Qingshan Deng

et al.

Frontiers in Endocrinology, Journal Year: 2025, Volume and Issue: 16

Published: March 24, 2025

Background Smoking is a global public health concern, with approximately 1,245 billion smokers worldwide. It associated range of complications, including cardiovascular and respiratory diseases. Osteoporosis, characterized by reduced bone density deterioration tissue, has prevalence 18.3%, higher rates in women over the age 50. been recently osteoporosis, potentially due to shared metabolic disorders or personal habits. This study aimed investigate association between smoking osteoporosis relation all-cause mortality cohort from United States. Methods Data were sourced National Health Nutrition Examination Survey (NHANES) database, which focuses on individuals aged 20 years older 2005–2010, 2013–2014, 2017–2018, where femoral neck testing was conducted. The participants categorized basis their self-reported status mineral (BMD) measurements, following World Organization criteria for osteoporosis. covariates included age, sex, race, alcohol consumption, BMI, blood glucose levels, other indicators. Statistical analysis ANOVA chi-square tests baseline characteristics, Kaplan–Meier survival analysis, multivariate Cox regression assess hazard ratios (HRs) 95% confidence intervals (CIs) mortality. We divided patients into four different groups via cross-classification method whether they had Results 19,400 participants, significant differences characteristics across 4 (S-/OP+: nonsmokers osteoporosis; S+/OP-: without S-/OP-: S+/OP+: osteoporosis). overall average 53.1 years, accounted 49.6% total population. rate all factors population 13.1%, highest S+/OP+ rate. Participants both history 146% increase (HR: 2.46, CI: 2.12–2.87) even after adjusting confounding factors. relative excess risk interaction (RERI) suggested lack statistical significance, whereas attributable proportion (AP) indicated synergistic effect Conclusions highlights importance managing preventing reduce findings provide preliminary evidence risk, emphasizing need proactive strategies cessation close monitoring conditions.

Language: Английский

Citations

0
Smoking, Genetic Susceptibility and Early Menopause: Unveiling Biological Mechanisms and Potential Therapy Targets DOI
Yuhang Liang, Jie Ou,

Jing Fu

et al.

BJOG An International Journal of Obstetrics & Gynaecology, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 27, 2024

ABSTRACT Objective To explore the association between smoking, genetic susceptibility and early menopause (EM) clarify potential mechanisms underlying this relationship. Design An observational Transcriptome‐wide analysis (TWAS) study. Setting UK Biobank public summary statistics. Population 139 869 women with full baseline data, no gynaecological surgery history. Methods Adjusted modified Poisson regression models were developed to determine smoking risk effects on EM. TWAS was used identify gene expression EM, Mendelian randomisation (MR) infer causality. Enrichment explored regulatory networks of transcription factors, microRNAs therapeutic targets. Small molecule drugs predicted using drug‐gene interaction analysis. Main Outcome Measures EM prevalence common patterns. Results Women over 30 pack‐years had about 1.5 times higher risk, RRs 1.39 (95%CI, 1.23–1.56), 1.45 (1.33–1.59) (1.36–1.55) in low, intermediate high groups. identified hub genes such as IMMP2L, BMPR2 HMGN1. MR confirmed daily cigarette consumption a causal factor menopause. Several targets (e.g., SP600125, INCB18424 ruxolitinib) identified. Conclusions Smoking reduction significantly lowered Hub provided new avenues for mitigating harmful smoking.

Language: Английский

Citations

2