Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Zingerone Facilitates Apoptosis in Triple Negative Breast Cancer Cells by Inducing Autophagy","authors":"Xia Cao,&nbsp;Chien-Wei Chen,&nbsp;Kai Yin,&nbsp;Tzong-Luen Wang,&nbsp;Yao-Kuang Huang,&nbsp;Pang-Yen Chen,&nbsp;Po-Hua Su","doi":"10.1002/jbt.70074","DOIUrl":"https://doi.org/10.1002/jbt.70074","url":null,"abstract":"<div>\u0000 \u0000 <p>Triple negative breast cancer (TNBC) is characterized by high heterogenicity and aggressiveness and autophagy plays a complicated role in cancer development. Zingerone is reported to possess multiple pharmacological activities, including antitumors. This study explored the biological role and the relevant mechanisms of zingerone in TNBC. Following zingerone treatment, the viability of normal breast cancer cells MCF-10A and TNBC cells (MDA-MB-231 and MDA-MB-468) was detected with CCK-8 assay. The proliferation, migration and invasion of TNBC cells were detected with colony formation, wound healing, and transwell assays. Western blot was used to detect the expressions of migration-, apoptosis- and autophagy-related proteins. Flow cytometry was used to detect the cell apoptotic level and immunofluorescence assay measured the autophagy. The experimental data revealed that zingerone with varying concentrations suppressed cell viability, proliferation, migration and invasion while promoting the apoptosis in TNBC, which might be mediated by autophagy activation. Besides, zingerone decreased HDAC1 expression in TNBC cells and regulated autophagy via HDAC1. Collectively, zingerone impeded the malignant progression of TNBC via inducing HDAC1-mediated autophagy.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142762517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FOXD2-AS1 Binding to MYC Activates EGLN3 to Affect the Malignant Progression of Clear Cell Renal Cell Carcinoma","authors":"Zhigang Huang,&nbsp;Bin Liu,&nbsp;Xiaoju Li,&nbsp;Chenghua Jin,&nbsp;Quansen Hu,&nbsp;Zhiwei Zhao,&nbsp;Qian Wang","doi":"10.1002/jbt.70083","DOIUrl":"https://doi.org/10.1002/jbt.70083","url":null,"abstract":"<div>\u0000 \u0000 <p>Long noncoding RNA (lncRNA) FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) show high expression in various cancers with elusive regulatory mechanisms. This study investigated the regulatory mechanism of FOXD2-AS1 in clear cell renal cell carcinoma (ccRCC) and its influence on ccRCC cell functions, providing novel insights into ccRCC treatment and a theoretical basis for refining prognoses of ccRCC patients.</p>\u0000 <p>Through differential analysis and survival analysis, differentially expressed lncRNAs (DElncRNAs) that were significantly linked with the prognosis of ccRCC were initially identified, and lncRNA-transcription factor-mRNA triplet was predicted via lncMAP database. RNA immunoprecipitation, chromatin immunoprecipitation, and dual-luciferase reporter assays were applied to verify the targeted relationship between MYC, FOXD2-AS1, and Egl-9 family hypoxia-inducible factor 3 (EGLN3). Cell functions in ccRCC were detected by a set of cell functional assays. Mice experiment was utilized for in vivo validation.</p>\u0000 <p>We uncovered the elevated FOXD2-AS1 and EGLN3 expression in ccRCC, as well as the promotion effect of FOXD2-AS1 on ccRCC cells to proliferate, migrate, and invade via upregulating EGLN3 expression. Our results also suggested that the regulatory influence of FOXD2-AS1 on EGLN3 was achieved by recruiting MYC to the EGLN3 promoter region. <i>In vitro</i> and in vivo assays both confirmed that the FOXD2-AS1/MYC/EGLN3 axis could accelerate the progression of ccRCC.</p>\u0000 <p>FOXD2-AS1 activated EGLN3 to accelerate ccRCC cell functions via binding to the transcription factor MYC.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142762515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANRIL's Epigenetic Regulation and Its Implications for Cardiovascular Disorders","authors":"Ehssan Moglad,&nbsp;Parjinder Kaur,&nbsp;Soumya V. Menon,&nbsp; Abida,&nbsp;Haider Ali,&nbsp;Mandeep Kaur,&nbsp;Mahamedha Deorari,&nbsp;Kumud Pant,&nbsp;Waleed Hassan Almalki,&nbsp;Imran Kazmi,&nbsp;Sami I. Alzarea","doi":"10.1002/jbt.70076","DOIUrl":"https://doi.org/10.1002/jbt.70076","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiovascular disorders (CVDs) are a major global health concern, but their underlying molecular mechanisms are not fully understood. Recent research highlights the role of long noncoding RNAs (lncRNAs), particularly ANRIL, in cardiovascular development and disease. ANRIL, located in the human genome's 9p21 region, significantly regulates cardiovascular pathogenesis. It controls nearby tumor suppressor genes CDKN2A/B through epigenetic pathways, influencing cell growth and senescence. ANRIL interacts with epigenetic modifiers, leading to altered histone modifications and gene expression changes. It also acts as a transcriptional regulator, impacting key genes in CVD development. ANRIL's involvement in cardiovascular epigenetic regulation suggests potential therapeutic strategies. Manipulating ANRIL and its associated epigenetic modifiers could offer new approaches to managing CVDs and preventing their progression. Dysregulation of ANRIL has been linked to various cardiovascular conditions, including coronary artery disease, atherosclerosis, ischemic stroke, and myocardial infarction. This abstract provides insights from recent research, emphasizing ANRIL's significance in the epigenetic landscape of cardiovascular disorders. By shedding light on ANRIL's role in cellular processes and disease development, the abstract highlights its potential as a therapeutic target for addressing CVDs.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142762078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon Induced Upregulation of Tripartite Motif 34 (TRIM34) Leads Apoptotic Cell Death in Lung Adenocarcinoma","authors":"Kaushalkumar Chaudhari,&nbsp;Vihas T. Vasu,&nbsp;Aparna Golani,&nbsp;Afridi Shaikh,&nbsp;Nidhi Nagariya,&nbsp;Hetal Roy","doi":"10.1002/jbt.70072","DOIUrl":"10.1002/jbt.70072","url":null,"abstract":"<div>\u0000 \u0000 <p>Despite breakthroughs in our understanding of lung cancer risk, development, immunologic control, and therapy choices, it remains one of the leading causes of cancer mortality. This study aimed to investigate the role of TRIM34 upon treatment of Interferon Gamma (IFN-γ) in Non-Small Cell Lung Cancer (NSCLC). NCI-H23 cells were exposed to IFN-γ in a dose- and time-dependent manner to understand TRIM34 expression and its role as a co-regulator of treatment. The regulatory role of TRIM34 on IFN-γ exposure was studied by qRT-PCR, Western blot analysis, immunocytochemistry, apoptosis assay and scratch assay. On exposure to IFN-γ, TRIM34 expression at transcript and protein level was significantly upregulated. With its upregulation, NCI-H23 underwent apoptosis and its rate of proliferation was impeded. Our results suggest that induction of TRIM34 by IFN-γ treatment may lead to an anti-tumor inflammatory response, resulting in NSCLC regression via apoptosis.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotine and Vape: Drugs of the Same Profile Flock Together","authors":"Titilayomi A. Otenaike,&nbsp;Oluwabukola M. Farodoye,&nbsp;Monica M. de Silva,&nbsp;Julia S. Loreto,&nbsp;Adeola O. Adedara,&nbsp;Matheus M. dos Santos,&nbsp;Alessandro S. de Prestes,&nbsp;Nilda V. Barbosa,&nbsp;João B. T. da Rocha,&nbsp;Luiz E. Lobo,&nbsp;Roger Wagner,&nbsp;Amos O. Abolaji,&nbsp;Elgion L. S. Loreto","doi":"10.1002/jbt.70075","DOIUrl":"https://doi.org/10.1002/jbt.70075","url":null,"abstract":"<div>\u0000 \u0000 <p>Smoking, a major behavioral health burden, causes preventable and premature deaths globally. Nicotine, the addictive component present in tobacco products and Electronic cigarettes (E-cigarettes, vape), can bind to nicotinic acetylcholine receptors in the brain to trigger a dopamine release that reinforces smoking. Despite the widespread usage of nicotine, its mechanisms of toxicity, particularly in e-cigarettes, are poorly understood. Using <i>Drosophila melanogaster</i> as a model organism, this study aims to investigate the mechanism of the toxicity of nicotine and vape. Behavioral parameters, oxidative stress indicators, mRNA expression levels of Dopamine 1- receptor 1 (Dop1R1), Acetyl-coenzyme A synthetase (AcCoAs), and apoptotic proteins were assessed in the flies after a 5-day exposure to varying concentrations of nicotine (0.15, 0.25, and 0.35 mg/mL diet) and vape (0.06, 0.08, and 0.12 mg/mL diet). Furthermore, Gas Chromatography-Mass Spectrometry (GC/MS) and Gas Chromatography-Flame Ionization Detection (GC/FID) analyzes were conducted to gain more insight on the composition of the vape used in study. Findings indicate that both nicotine and vape exposure significantly reduced lifespan, impaired locomotor activity, and disrupted sleep patterns. Notably, nicotine exposure stimulated <i>Dop1R1</i> transcription and altered <i>Acetyl-CoA</i> gene expression, impacting the viability and behavior of the flies. Elevated levels of reactive oxygen biomarkers were observed, contributing to cellular damage through oxidative stress and apoptotic mechanisms mediated by the <i>Reaper</i> and <i>DIAP1</i> proteins. Additionally, the composition analysis of vape liquid revealed the presence of propylene glycol, nicotine, methyl esters, and an unidentified compound. This study highlights the complex interplay between nicotine, gene expression, and physiological responses in <i>Drosophila</i>.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing Outcomes in Heart Transplantation: The Role of High-Intensity Statin Therapy","authors":"Nima Ghavamikia,&nbsp;Hossein Saffarfar,&nbsp;Babak Seifdavati,&nbsp;Mohaddeseh Jamali,&nbsp;Shadi Izadidehkordi,&nbsp;Seyyed Abbas Pakmehr,&nbsp;Mohammadreza Aghabali,&nbsp;Negar Jahani,&nbsp;Payam Ali-Khiavi,&nbsp;Abtin Soleimanian,&nbsp;Ahmed Hijazi,&nbsp;Milad Vahedinezhad,&nbsp;Reza Shahhoseini","doi":"10.1002/jbt.70070","DOIUrl":"https://doi.org/10.1002/jbt.70070","url":null,"abstract":"<div>\u0000 \u0000 <p>Heart transplantation is a vital procedure for patients with end-stage heart failure, but it faces significant challenges, including graft dysfunction, rejection, and cardiac allograft vasculopathy (CAV), which can compromise long-term graft success. Research suggests that statin therapy may offer significant benefits to heart transplant recipients, such as improved long-term survival and reduced rates of graft rejection and mortality. The aim of this review is to thoroughly examine the recent literature on this topic since 2005. Early use of high-dose statins appears to be particularly effective in preventing vasculopathy and improving outcomes, although a titrated approach may help to reduce side effects. High-dose statins may provide superior cardiovascular benefits, including lower rates of CVD, slower progression of CVD and improved long-term graft survival. Despite potential concerns about adverse effects, evidence suggests that high-intensity statins improve cholesterol levels without increasing serious adverse events after transplantation. The goal of statin therapy in heart transplant recipients is to balance the well-established benefits seen in the general population with the specific needs of this group, with the ultimate goal of improving both longevity and quality of life.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA circ_0004630 promotes malignancy and glycolysis of nonsmall cell lung cancer by sponging microRNA-1208 and regulating leucine-rich repeat kinase 2 expression","authors":"Xiangli Zhang,&nbsp;Junfang Wu,&nbsp;Yi Miao,&nbsp;Jing Wang,&nbsp;Enguang Wang","doi":"10.1002/jbt.23811","DOIUrl":"https://doi.org/10.1002/jbt.23811","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Emerging evidence has discovered that circular RNAs play important regulators of nonsmall cell lung cancer (NSCLC), but the role and potential molecular mechanism of hsa_circ_100549 (circ_0004630) involved in NSCLC is poorly defined. In this study, circ_0004630, microRNA-1208 (miR-1208), and leucine-rich repeat kinase 2 (LRRK2) expression were detected using real-time quantitative polymerase chain reaction. Cell proliferation, colony formation, apoptosis, and invasion were assessed using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2’-deoxyuridine, colony formation, flow cytometry, and transwell assays. Protein levels of glucose transporter 1, Hexokinase 2, and LRRK2 were detected using western blot assay. Glucose consumption, lactate production, and adenosine triphosphate content were assessed using the corresponding kits. After predicting via bioinformatics software Circinteractome and Targetscan, the binding between miR-1208 and circ_0004630 or LRRK2 was verified by a dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assay. The xenograft tumor model analyzed the biological role circ_000460 on tumor growth <i>in vivo.</i> It was found that circ_0004630 and LRRK2 were increased, and miR-1208 was low expression in NSCLC tissues and cells. Functionally, the downregulation of circ_0004630 inhibited NSCLC cell proliferation, invasion, glycolysis, and accelerated apoptosis in vitro. In mechanism, circ_0004630 might work as a sponge of miR-1208 to modulate LRRK2 expression. In addition, DUXAP8 deficiency cured neuroblastoma tumor growth in vivo. In conclusion, circ_0004630 knockdown might suppress NSCLC cell proliferation, metastasis, and glycolysis partly by the miR-1208/LRRK2 axis. Our findings hinted at an important theoretical basis for further elucidating the pathogenesis of NSCLC and targeted therapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Embryonic Flubendiamide Exposure Alters Expression of OTX2 and Other Early Regulators in Domestic Chick Leading to Congenital Eye Defects","authors":"Dhanush Danes,&nbsp;Bhaval Parmar,&nbsp;Juhi Vaishnav,&nbsp;Shweta Umar,&nbsp;Shashikant Sharma,&nbsp;Suresh Balakrishnan","doi":"10.1002/jbt.70067","DOIUrl":"10.1002/jbt.70067","url":null,"abstract":"<div>\u0000 \u0000 <p>Flubendiamide, a phthalic acid diamide insecticide, has been implicated in potential teratogenic effects on non-target organisms, especially during embryonic development. This study examines the impact of flubendiamide on eye development in chick embryos, a well-established model for vertebrate development. Exposure to 0.5 µg/µL of flubendiamide significantly impaired early ocular morphogenesis, resulting in severe defects such as underdeveloped optic cups and the absence of lens and corneal structures. Histopathological analysis demonstrated disrupted optic cup differentiation, while in silico docking studies revealed strong interactions between flubendiamide and key oculogenic proteins, including OTX2, PAX6, and SOX2. These interactions were associated with altered expression patterns of these critical regulators, alongside overexpression of SHH and downregulation of BMP4, BMP7, and FGF8, which are essential for optic vesicle formation and lens differentiation. Additionally, increased CASPASE-3 expression indicated enhanced apoptosis, contributing to the observed ocular anomalies. These findings suggest that flubendiamide disrupts key signaling pathways necessary for proper eye development, potentially leading to congenital eye defects. The study highlights the need for a thorough evaluation of the molecular mechanisms driving flubendiamide-induced teratogenicity to ensure safer pesticide use and protect environmental and human health.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of PD-1 in modulating IFN-γ-CXCL9/10-CXCR3 signaling in breast cancer","authors":"Lei Hong,&nbsp;Fang Huang,&nbsp;Zexian Hu,&nbsp;Qian Dong,&nbsp;Yan Kong,&nbsp;Xuan Zheng,&nbsp;Man Li,&nbsp;Yanzhi Cui","doi":"10.1002/jbt.23842","DOIUrl":"10.1002/jbt.23842","url":null,"abstract":"<p>Breast cancer represents a significant health burden globally, necessitating ongoing advancements in treatment strategies for improved patient outcomes. Immunotherapy, particularly targeting immune checkpoints like programmed death-1 (PD-1), has emerged as a promising approach in cancer therapy. This study focuses on elucidating the role of PD-1 in modulating the IFN-γ-CXCL9/10-CXCR3 signaling axis within the breast cancer microenvironment. By investigating the synergistic effects of PD-1 inhibitors in combination with Inetetamab, our research aims to uncover novel therapeutic targets for enhancing immunotherapy efficacy in breast cancer. Through comprehensive experimental analysis, we seek to deepen our understanding of the intricate molecular mechanisms underlying immune regulation in breast cancer, thereby paving the way for more effective and sustainable treatment strategies. Ultimately, our study endeavors to establish a robust theoretical framework that can guide the development of innovative clinical interventions, aiming for improved outcomes in breast cancer patients.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autophagy in the Cellular Consequences of Tobacco Smoking: Insights into Senescence","authors":"Maryam Akhtari,&nbsp;Mobina Jalalvand,&nbsp;Makan Sadr,&nbsp;Hooman Sharifi","doi":"10.1002/jbt.70065","DOIUrl":"10.1002/jbt.70065","url":null,"abstract":"<div>\u0000 \u0000 <p>Smoking is a significant contributing factor to the development of many complex diseases. One of the most important stimuli for aging in the human body is constant exposure to environmental factors such as cigarette smoke. Free radicals in cigarette smoke cause reactive oxygen species production at the cellular level and induce inflammatory responses. The respiratory system of smokers exhibits age-related characteristics, such as enhanced oxidative stress, accumulated damaged proteins, and increased inflammation. Autophagy is triggered by tobacco smoke as a protective mechanism to prevent and reduce molecular stress. However, smoking can interfere with the normal functioning of autophagy in various ways. Smoking-induced impairment of autophagy leads to irreversible cellular damage accumulation, causing cells to undergo cellular aging or senescence. Senescent cells lose their ability to divide and display a distinct secretory phenotype called the senescence-associated secretory phenotype (SASP) and produce numerous growth factors, immune modulators, and inflammatory cytokines. This review discusses the effects of tobacco smoke exposure on autophagy alteration, cellular aging, and senescence induction in exposed animal models, as well as in exposed epithelial and immune cells in the body.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}