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Role of Mitochondria in the Chronification of Inflammation: Focus on Dysfunctional Mitophagy and Mitochondrial DNA Mutations 线粒体在炎症慢性化中的作用：聚焦功能失调的线粒体吞噬和线粒体 DNA 突变

Gene Expression Pub Date : 2023-11-30 DOI: 10.14218/ge.2023.00061

Alexander N. Orekhov, Volha I. Summerhill, V. Khotina, Mikhail A. Popov, Jamol K. Uzokov, V. Sukhorukov

{"title":"Role of Mitochondria in the Chronification of Inflammation: Focus on Dysfunctional Mitophagy and Mitochondrial DNA Mutations","authors":"Alexander N. Orekhov, Volha I. Summerhill, V. Khotina, Mikhail A. Popov, Jamol K. Uzokov, V. Sukhorukov","doi":"10.14218/ge.2023.00061","DOIUrl":"https://doi.org/10.14218/ge.2023.00061","url":null,"abstract":"Inflammation is a natural reaction of the innate immune system that evolved primarily to protect the human body from invading pathogens and to heal injuries. There are two different types of inflammation, acute and chronic inflammation, differing in duration, underlying causes, and characteristics. The acute-to-chronic transition can be determined by several pathomech-anisms, including dysregulation of immune response and failure to eliminate the underlying cause. Moreover, epigenetic changes that refer to modifications in gene expression that are heritable but do not involve changes to the underlying DNA sequence can also contribute to prolonged inflammation. Emerging evidence suggests that dysfunctional mitochondria can promote the development of chronic inflammation. In this respect, the mechanisms triggering defective mitophagy, a selective form of autophagy that exterminates dysfunctional mitochondria to maintain cellular homeostasis, attracted special attention. The hypothesis on the pivotal role of mutations in mitochondrial DNA causing defective mitophagy stimulated the area of the research that applies editing of the mitochondrial genome. The mitoCAS9 vector and two single guide RNAs to the G15059A mutation were used to eliminate the mutation from the macrophage-like cells. The normal activity of the initially defective mitophagy was restored in intact macrophage-like cells, confirming the causal role of the G15059A mutation in the disruption of the mitophagy process. The unraveling of the underlying mechanisms of chronic inflammation will help to develop targeted therapeutic approaches aimed at restoring mitochondrial health and alleviating chronic inflammation that can be used for the treatment of a wide range of chronic inflammatory diseases.","PeriodicalId":502456,"journal":{"name":"Gene Expression","volume":"602 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139202927","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}

引用次数: 0

An Ensemble Learning-based Framework from Multicohort Reveals the Molecular Mechanism of GREM1 in Endometrial Cancer 基于集合学习的多队列框架揭示了 GREM1 在子宫内膜癌中的分子机制

Gene Expression Pub Date : 2023-11-30 DOI: 10.14218/ge.2023.00095

Yihao Zhu, Hui Wang, Yao Zu

引用次数: 0

Interleukin 17F Gene Polymorphisms and Chronic Kidney Allograft Failure 白细胞介素 17F 基因多态性与慢性肾移植失败

Gene Expression Pub Date : 2023-11-30 DOI: 10.14218/ge.2023.00099

A. Liacini, D. Olwi, Gaurav Tripathi, R. Faridi, Faisal Khan, A. Sar, Serdar Yilmaz, N. Berka

{"title":"Interleukin 17F Gene Polymorphisms and Chronic Kidney Allograft Failure","authors":"A. Liacini, D. Olwi, Gaurav Tripathi, R. Faridi, Faisal Khan, A. Sar, Serdar Yilmaz, N. Berka","doi":"10.14218/ge.2023.00099","DOIUrl":"https://doi.org/10.14218/ge.2023.00099","url":null,"abstract":"Background and objectives: Polymorphisms of the interleukin (IL)-17 proinflammatory cytokine family (IL17A and IL17F) have been associated with kidney chronic allograft failure (CAF). To date, the impact of heritable differences in IL17F genes and CAF among kidney transplant patients from North America has not been reported. The objective of the study was to assess the association of five distinct polymorphisms in the IL17F gene with histopathological changes in chronic kidney allograft failure. Methods: Two hundred eighteen kidney transplant recipients were enrolled. Surveillance biopsies were performed to evaluate 11 distinct histological markers and the combined grade of interstitial fibrosis and tubular atrophy, 6 to 12 months post-transplant. Using direct sequencing, the IL17F polymorphisms (-1507C/T rs1889570, -1165A/G rs1266828, -5046C/T rs7771511, -6328G/A rs766748, and -7488A/G rs763780) were genotyped in the 10 healthy volunteer samples followed by all kidney transplant recipients were genotyped for five IL17F gene polymorphisms using polymerase chain reaction and sequence-specific primers. The association was evaluated using both univariate and multivariate logistic regression analysis. Results: We observed weak associations of TC genotype of IL17F - 1165 (rs1266828) and allele of IL17F -1507C (rs1889570) with glomerular sclerosis and interstitial fibrosis and tubular atrophy ( p = 0.017 and p = 0.03) respectively. Allele C of IL-17 -1165C/T (rs1266828) was associated with better glomerular sclerosis ( p = 0.004, odds ratio = 0.39) score. Conclusions: Our findings demonstrate that IL17F SNPs were not associated with CAF and support our prior published results","PeriodicalId":502456,"journal":{"name":"Gene Expression","volume":"127 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139197171","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}

引用次数: 0

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