DNA and cell biologyPub Date : 2024-12-01Epub Date: 2024-11-06DOI: 10.1089/dna.2024.0122
Chenlingzi Huang, Lujiadai Xue, Xinzi Lin, Yuan Shen, Xiaoyu Wang
{"title":"Histone Lactylation-Driven GPD2 Mediates M2 Macrophage Polarization to Promote Malignant Transformation of Cervical Cancer Progression.","authors":"Chenlingzi Huang, Lujiadai Xue, Xinzi Lin, Yuan Shen, Xiaoyu Wang","doi":"10.1089/dna.2024.0122","DOIUrl":"10.1089/dna.2024.0122","url":null,"abstract":"<p><p>Cervical cancer (CC) is the most common cancer in women. This study aims to explore the molecular mechanism of lactate secreted by CC cells modulating macrophage polarization in CC via histone lactylation. Normal cervical epithelium (NCE), low-grade squamous intraepithelial lesion (LSIL), high-grade squamous intraepithelial lesion (HSIL), and cervical squamous cell carcinoma (CESC) were collected to assess H3K18la level and macrophage infiltration. Macrophages were incubated with SiHa cell-derived conditioned medium to detect M1 and M2 markers. NCE, HSIL, and CESC samples were used for ChIP-seq of H3K18la. Histone lactylation-dirven <i>GPD2</i> was knocked down in macrophages. Compared to NCE, H3K18la level and M2 macrophage abundance were increased in LSIL, HSIL, and CESC. Lactate secreted by CC cells upregulated H3K18la and M2 markers but downregulated M1 markers in macrophages. ChIP-seq revealed that upregulated pathways in HSIL vs. NCE and CESC vs. HSIL were commonly enriched in lipid metabolism. Notably, lactate upregulated H3K18la-modified <i>GPD2</i> expression in macrophages, and <i>GPD2</i> knockdown reversed lactate induction to M2 macrophages. Collectively, lactate secreted by CC cells upregulates <i>GPD2</i> via histone lactylation, thereby promoting M2 macrophage polarization in CC. This study provides new insights into the role of histone lactylation in macrophage polarization in the malignant transformation of CC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"605-618"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DNA and cell biologyPub Date : 2024-12-01Epub Date: 2024-10-21DOI: 10.1089/dna.2024.0173
Kenneth Rubio-Carrasco, Paola García de la Torre, José D Martínez-Ezquerro, Sergio Sánchez-García, Elisa García-Vences, Ignacio Camacho-Arroyo, Mauricio Rodríguez-Dorantes, Vanessa González-Covarrubias
{"title":"Hypertension Control Is Associated with Telomere Length in Older Adults.","authors":"Kenneth Rubio-Carrasco, Paola García de la Torre, José D Martínez-Ezquerro, Sergio Sánchez-García, Elisa García-Vences, Ignacio Camacho-Arroyo, Mauricio Rodríguez-Dorantes, Vanessa González-Covarrubias","doi":"10.1089/dna.2024.0173","DOIUrl":"10.1089/dna.2024.0173","url":null,"abstract":"<p><p>Hypertension is the leading risk for cardiovascular disease and worldwide mortality. Uncontrolled blood pressure worsens with age and its control is part of public health strategies especially for older adults. Telomere length (TL) has been associated with hypertension, with age and sex as relevant confounding factors, but it is not clear whether hypertension control in older adults impacts on TL and if this relationship is consistently age and sex dependent. TL was assessed in leukocytes of 369 hypertensive patients. Individuals were >60 years male (169) and female (200) and have been diagnosed and treated for hypertension for at least four years. TL was measured by RT-PCR using a commercial probe. Regression models were developed considering systolic and diastolic blood pressure control as dependent variables and age, sex, glucose, and lipid levels as confounding factors. TL showed a mean of 7.5 ± 5.1 Kb, and no difference between males and females was observed. We identified a significant association between systolic blood pressure control and TL (<i>p</i> value = 0.039) and a trend for diastolic blood pressure (<i>p</i> value = 0.061). These observations confirm and expand previous reports showing that hypertension control can have an impact on TL and consequently on other factors of healthy aging.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"571-578"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Impact of Chondroitin Sulfate Proteoglycan 4 Pseudogene 12 Genetic Variants on Colorectal Cancer Risk: A Case-Control Study.","authors":"Xianlei Zhou, Liwen Guo, Zhenbang Yang, Hongxue Xu, Zhi Zhang, Xuemei Zhang","doi":"10.1089/dna.2024.0174","DOIUrl":"10.1089/dna.2024.0174","url":null,"abstract":"<p><p>This study aims to investigate the correlation between the chondroitin sulfate proteoglycan 4 pseudogene 12 (<i>CSPG4P12</i>) polymorphism and the risk of colorectal cancer (CRC). This case-control study involved 850 patients with CRC and 850 health controls. The genotypes of <i>CSPG4P12</i> (rs2880765, rs6496932, and rs8040855) were determined by the TaqMan-MGB probe method. Logistic regression model was employed to evaluate the association of <i>CSPG4P12</i> single-nucleotide polymorphisms (SNPs) with the risk of CRC by calculating the odds ratio (OR) and 95% confidence interval (CI). The <i>CSPG4P12</i> exhibited lower expression in CRC tissues. Our data showed that the rs6496932 variant increased CRC risk (CA vs. CC: <i>p</i> = 0.006; CA + AA vs. CC: <i>p</i> = 0.005). In contrast, the rs8040855 variant reduced the risk of CRC (CG vs. CC: <i>p</i> < 0.001; CG + GG vs. CC: <i>p</i> < 0.001). Stratification by gender and age revealed that the rs8040855 variant decreased CRC risk; however, the rs6496932 variant increased CRC risk among males (CA vs. CC: <i>p</i> = 0.024; CA + AA vs. CC: <i>p</i> = 0.014) and younger individuals (CA vs. CC: <i>p</i> = 0.004; CA + AA vs. CC: <i>p</i> = 0.010). When stratified by smoking and drinking status, the rs8040855 variant decreased CRC risk among nonsmokers (CG vs. CC: <i>p</i> < 0.001; CG + GG vs. CC: <i>p</i> < 0.001) and nondrinkers (CA vs. CC: <i>p</i> = 0.002; CA + AA vs. CC: <i>p</i> = 0.004). The rs6496932 variant increased CRC risk among nonsmokers (CA vs. CC: <i>p</i> = 0.016; CA + AA vs. CC: <i>p</i> = 0.036) and nondrinkers (CG vs. CC: <i>p</i> < 0.001; CG + GG vs. CC: <i>p</i> < 0.001). Haplotype analysis showed that the <i>CSPG4P12</i> T<sub>rs2880765</sub>C<sub>rs6496932</sub>G<sub>rs8040855</sub> haplotype reduced the risk of CRC compared with the reference haplotype (<i>CSPG4P12</i> A<sub>rs2880765</sub>C<sub>rs6496932</sub>C<sub>rs8040855</sub>) (OR = 0.46, 95% CI = 0.26-0.82, <i>p</i> = 0.049). These findings highlight the potential of these genetic variants as biomarkers for CRC susceptibility, offering insights into personalized prevention strategies.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"596-604"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DNA and cell biologyPub Date : 2024-11-01Epub Date: 2024-10-15DOI: 10.1089/dna.2024.0107
Yiyu Qin, Yang Zhou, Hongyan Wu, Haiming Lei, Tingyu Ding, Xinya Shen, Jian Li
{"title":"SNORA71A Downregulation Enhances Gemcitabine Sensitivity in Gallbladder Cancer Cells by Inducing Ferroptosis Through Inhibiting the AKT/NRF2/GPX4 Pathway.","authors":"Yiyu Qin, Yang Zhou, Hongyan Wu, Haiming Lei, Tingyu Ding, Xinya Shen, Jian Li","doi":"10.1089/dna.2024.0107","DOIUrl":"10.1089/dna.2024.0107","url":null,"abstract":"<p><p>Previous findings have indicated a marked upregulation of SNORA71A in gallbladder cancer (GBC) tissues compared to normal samples. However, the precise role and molecular mechanisms of SNORA71A in GBC remain largely unknown. Moreover, gemcitabine (GEM) drug resistance has been found to lead to unfavorable outcomes and recurrence in GBC patients. Therefore, this study aims to investigate the impact of SNORA71A on GBC and explore its potential effects on the sensitivity of GBC cells to GEM. RT-qPCR was conducted to assess SNORA71A level in matched normal and GBC tissues. Cell proliferation was examined through CCK-8 and 5-ethynyl-2'-deoxyuridine (EdU) assays. Additionally, the expression of proteins in GBC cells was analyzed using western blot assay. The level of SNORA71A was notably higher in GBC tissues relative to normal tissues. SNORA71A overexpression led to increased GBC cell proliferation and invasion. Conversely, SNORA71A deficiency strongly suppressed GBC cell proliferation and invasion and triggered cell apoptosis and ferroptosis. Additionally, downregulation of SNORA71A obviously enhanced the antiproliferative and anti-invasive effects of GEM on GBC cells, whereas these changes were reversed by inhibiting ferroptosis. Furthermore, deficiency of SNORA71A further augmented the GEM-induced downregulation of p-Akt, Nrf2, and GPX4 in NOZ cells; however, these effects were reversed by ferroptosis inhibition. Collectively, these findings suggested that downregulation of SNORA71A may increase the sensitivity of GBC cells to GEM by triggering ferroptosis through inhibiting the AKT/NRF2/GPX4 signaling pathway.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"559-569"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DNA and cell biologyPub Date : 2024-11-01Epub Date: 2024-09-05DOI: 10.1089/dna.2024.0105
Dandan Gao, Heng Zhang, Wanjun Sun, Huaqing Wang, Hui Wang
{"title":"Radiation-Induced Intestinal Injury: Molecular Mechanisms and Therapeutic Status.","authors":"Dandan Gao, Heng Zhang, Wanjun Sun, Huaqing Wang, Hui Wang","doi":"10.1089/dna.2024.0105","DOIUrl":"10.1089/dna.2024.0105","url":null,"abstract":"<p><p>Radiation-induced intestinal injury is one of the most common intestinal complications caused by pelvic and abdominal tumor radiotherapy, severely impacting patients' quality of life. Ionizing radiation, while killing tumor cells, inevitably damages healthy tissue. Radiation-induced enteropathy results from radiation therapy-induced intestinal tissue damage and inflammatory responses. This damage involves various complex molecular mechanisms, including cell apoptosis, oxidative stress, release of inflammatory mediators, disruption of immune responses, and imbalance of intestinal microbiota. A thorough understanding of these molecular mechanisms is crucial for developing effective prevention and treatment strategies.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"537-548"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DNA and cell biologyPub Date : 2024-11-01Epub Date: 2024-10-18DOI: 10.1089/dna.2024.0181
Reza Shah Hosseini, Seyed Mohammad Nouri, Pooja Bansal, Ahmed Hjazi, Harpreet Kaur, Anaheed Hussein Kareem, Abhinav Kumar, Rafil Adnan Hussein Al Zuhairi, Nadhim Allawi Al-Shaheri, Parya Mahdavi
{"title":"The p53/miRNA Axis in Breast Cancer.","authors":"Reza Shah Hosseini, Seyed Mohammad Nouri, Pooja Bansal, Ahmed Hjazi, Harpreet Kaur, Anaheed Hussein Kareem, Abhinav Kumar, Rafil Adnan Hussein Al Zuhairi, Nadhim Allawi Al-Shaheri, Parya Mahdavi","doi":"10.1089/dna.2024.0181","DOIUrl":"10.1089/dna.2024.0181","url":null,"abstract":"<p><p>One of the main health issues in the modern world is cancer, with breast cancer (BC) as one of the most common types of malignancies. Different environmental and genetic risk factors are involved in the development of BC. One of the primary genes implicated in cancer development is the p53 gene, which is also known as the \"gatekeeper\" gene. p53 is involved in cancer development by interacting with numerous pathways and signaling factors, including microRNAs (miRNAs). miRNAs are small noncoding RNA molecules that regulate gene expression by binding to the 3' untranslated region of target mRNAs, resulting in their translational inhibition or degradation. If the p53 gene is mutated or degraded, it can contribute to the risk of BC by disrupting the expression of miRNAs. Similarly, the disruption of miRNAs causes the negative regulation of p53. Therefore, the p53/miRNA axis is a crucial pathway in the progression or prevention of BC, and understanding the regulation and function of this pathway may contribute to the development of new therapeutic strategies to help treat BC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"549-558"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DNA and cell biologyPub Date : 2024-10-01Epub Date: 2024-08-12DOI: 10.1089/dna.2024.0119
Qi Zhou, Binlin Cai, Kun Liu, Hongxin Chen
{"title":"EIF4A3-Induced Upregulation of hsa_circ_0049396 Attenuates the Tumorigenesis of Nasopharyngeal Carcinoma by Regulating the Hippo-YAP Pathway.","authors":"Qi Zhou, Binlin Cai, Kun Liu, Hongxin Chen","doi":"10.1089/dna.2024.0119","DOIUrl":"10.1089/dna.2024.0119","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) and eukaryotic translation initiation factor 4A3 (EIF4A3) have been reported to participate in the pathogenesis of nasopharyngeal carcinoma (NPC), but their mechanism has not been fully understood. This research aimed to confirm the role and regulatory mechanism of hsa_circ_0049396 interacting with EIF4A3 in NPC tumorigenesis. Quantitative real time polymerase chain reaction (qRT-PCR) was executed to detect the levels of hsa_circ_0049396 and EIF4A3. Cell function experiments and nude mice xenograft assay were used to confirm the role of hsa_circ_0049396 in NPC. The regulatory effect of EIA4A3 on hsa_circ_0049396 was determined by circInteractome prediction, RNA binding protein immunoprecipitation (RIP) assay, and qRT-PCR. In addition, the Hippo-YAP pathway-related proteins and EIF4A3 protein were detected by western blotting. hsa_circ_0049396 was proved to be downregulated in NPC samples, and its low expression indicated the poor prognosis of NPC. After upregulating hsa_circ_0049396 in NPC cells, the proliferation, migration, invasion, and tumor growth <i>in vivo</i> were suppressed by inhibiting the Hippo-YAP pathway. Moreover, EIF4A3 bound to the flanking regions of the hsa_circ_0049396 to enhance hsa_circ_0049396 expression in NPC cells. hsa_circ_0049396 mediated by EIF4A3 in NPC can attenuate NPC tumorigenesis by inhibiting the Hippo-YAP pathway. This finding may provide a potential early diagnostic biomarker or drug target to improve the precision medicine approaches of NPC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"510-519"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141918389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DNA and cell biologyPub Date : 2024-10-01Epub Date: 2024-07-03DOI: 10.1089/dna.2024.0134
Sabrina N Kline, Yoshine Saito, Nathan K Archer
{"title":"<i>Staphylococcus aureus</i> Proteases: Orchestrators of Skin Inflammation.","authors":"Sabrina N Kline, Yoshine Saito, Nathan K Archer","doi":"10.1089/dna.2024.0134","DOIUrl":"10.1089/dna.2024.0134","url":null,"abstract":"<p><p>Skin homeostasis relies on a delicate balance between host proteases and protease inhibitors along with those secreted from microbial communities, as disruption to this harmony contributes to the pathogenesis of inflammatory skin disorders, including atopic dermatitis and Netherton's syndrome. In addition to being a prominent cause of skin and soft tissue infections, the gram-positive bacterium <i>Staphylococcus aureus</i> is a key player in inflammatory skin conditions due to its array of 10 secreted proteases. Herein we review how <i>S. aureus</i> proteases augment the development of inflammation in skin disorders. These mechanisms include degradation of skin barrier integrity, immune dysregulation and pruritis, and impairment of host defenses. Delineating the diverse roles of <i>S. aureus</i> proteases has the potential to reveal novel therapeutic strategies, such as inhibitors of proteases or their cognate target, as well as neutralizing vaccines to alleviate the burden of inflammatory skin disorders in patients.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"483-491"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11535466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141494576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Isoorientin Alleviates DSS-Treated Acute Colitis in Mice by Regulating Intestinal Epithelial P-Glycoprotein (P-gp) Expression.","authors":"Zhenzhen Wang, Lanzhu Yang, Yun Feng, Bensong Duan, Haibin Zhang, Yanru Tang, Caihang Zhang, Jingya Yang","doi":"10.1089/dna.2024.0101","DOIUrl":"10.1089/dna.2024.0101","url":null,"abstract":"<p><p>Isoorientin (ISO) is a naturally occurring flavonoid with diverse functional properties that mitigate the risk of diseases stemming from oxidation, inflammation, and cancer cell proliferation. P-glycoprotein (P-gp) is a vital component of the intestinal epithelium and may play a role in the onset of intestinal inflammatory conditions, such as inflammatory bowel disease (IBD). Recent studies have suggested that short-chain fatty acids (SCFAs) and secondary bile acids (SBAs) produced by the gut microbiota stimulate the increase of P-gp expression, alleviating excessive inflammation and thereby preservation of intestinal homeostasis. ISO has been shown to improve colon health and modulate the gut microbiota. In this study, we aimed to explore whether ISO can modulate the microbes and their metabolites to influence P-gp expression to alleviate IBD. First, the impact of ISO on dextran sulfate sodium (DSS)-treated colitis in mice was investigated. Second, 16S rRNA gene sequencing was conducted. The present study indicated that ISO mitigated the symptoms and pathological damage associated with DSS-treated colitis in mice. Western blot analysis revealed ISO upregulated P-gp in colon tissues, suggesting the critical role of P-gp protein in intestinal epithelial cells. 16S microbial diversity sequencing revealed ISO restored the richness and variety of intestinal microorganisms in colitis-bearing mice and enriched SCFA-producing bacteria, such as <i>Lachnospiraceae_NK4A136_group</i>. The experiments also revealed that the ISO fecal microbiota transplantation (FMT) inoculation of DSS-treated mice had similarly beneficial results. FMT mice showed a reduction in colitis symptoms, which was more pronounced in ISO-FMT than in CON-FMT mice. Meanwhile, ISO-FMT expanded the abundance of beneficial microorganisms, increased the expression of metabolites, such as SCFAs and total SBAs, and significantly upregulated the expression of P-gp protein. In addition, Spearman's correlation analysis demonstrated a positive correlation between the production of SCFAs and SBAs and the expression of P-gp. The present study identified that ISO increases the expression of P-gp in the intestinal epithelium by regulating intestinal microorganisms and their metabolites, which maintains colonic homeostasis, improves the integrity of the colonic epithelium, and alleviates colitis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"520-536"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"MiRNA Regulates Ferroptosis in Cardiovascular and Cerebrovascular Diseases.","authors":"Yiman Liu, Peijuan Yang, Jingjing Wang, Wu Peng, Jinli Zhao, Zuo Wang","doi":"10.1089/dna.2024.0135","DOIUrl":"https://doi.org/10.1089/dna.2024.0135","url":null,"abstract":"<p><p>Cardiovascular and cerebrovascular diseases (CCVDs) significantly contribute to global mortality and morbidity due to their complex pathogenesis involving multiple biological processes. Ferroptosis is an important physiological process in CCVDs, manifested by an abnormal increase in intracellular iron concentration. MiRNAs, a key class of noncoding RNA molecules, are crucial in regulating CCVDs through pathways like glutathione-glutathione peroxidase 4, glutamate/cystine transport, iron metabolism, lipid metabolism, and other oxidative stress pathways. This article summarizes the progress of miRNAs' regulation on CCVDs, aiming to provide insights for the diagnosis and treatment of CCVDs.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":"43 10","pages":"492-509"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}