Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease

Wu, Xun; Qin, Kele; Iroegbu, Chukwuemeka Daniel; Xiang, Kun; Peng, Jun; Guo, Jianjun; Yang, Jinfu; Fan, Chengming

doi:10.1111/jcmm.17239

Cited by 37 publications

(33 citation statements)

References 57 publications

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“…Nuclear receptor coactivator 4 (NCOA4) recognizes intracellular after ferritin recognition, and ferritin transfers stored ferric ions to the autophagosome for degradation, which, in turn, releases ferric ions into the cytoplasm to become free iron, a process also known as iron autophagy ( 59 , 60 ). In addition, genes such as nuclear receptor coactivator (NRF2) and heat shock protein B1 have been found to affect the sensitivity of cells to ferroptosis inducers by regulating intracellular iron ion metabolism ( 61 , 62 ). This shows that iron ion metabolism is a potential regulatory point for the induction of cellular ferroptosis.…”

Section: Ferroptosismentioning

confidence: 99%

Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer

Zhang

Liu

2022

Front. Immunol.

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Ovarian cancer (OC) is one of the most common malignancies that causes death in women and is a heterogeneous disease with complex molecular and genetic changes. Because of the relatively high recurrence rate of OC, it is crucial to understand the associated mechanisms of drug resistance and to discover potential target for rational targeted therapy. Cell death is a genetically determined process. Active and orderly cell death is prevalent during the development of living organisms and plays a critical role in regulating life homeostasis. Ferroptosis, a novel type of cell death discovered in recent years, is distinct from apoptosis and necrosis and is mainly caused by the imbalance between the production and degradation of intracellular lipid reactive oxygen species triggered by increased iron content. Necroptosis is a regulated non-cysteine protease–dependent programmed cell necrosis, morphologically exhibiting the same features as necrosis and occurring via a unique mechanism of programmed cell death different from the apoptotic signaling pathway. Pyroptosis is a form of programmed cell death that is characterized by the formation of membrane pores and subsequent cell lysis as well as release of pro-inflammatory cell contents mediated by the abscisin family. Studies have shown that ferroptosis, necroptosis, and pyroptosis are involved in the development and progression of a variety of diseases, including tumors. In this review, we summarized the recent advances in ferroptosis, necroptosis, and pyroptosis in the occurrence, development, and therapeutic potential of OC.

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Section: Ferroptosismentioning

confidence: 99%

Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer

Zhang

Liu

2022

Front. Immunol.

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“…The highlights of our study are the innovative combination of Lasso and RF methods and the excellent results produced in terms of predictive power. The feature selection method of Lasso (38)(39)(40)(41) and RF (42-45) has been widely used in biology as a way to better identify key biomarkers. Before that, there is still no study to construct a prediction model for SLE based on gene sequencing, especially since our study is based on whole blood samples from SLE patients, which are easy to obtain and manipulate.…”

Section: A B Cmentioning

confidence: 99%

Establishment and analysis of a disease risk prediction model for the systemic lupus erythematosus with random forest

et al. 2022

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Systemic lupus erythematosus (SLE) is a latent, insidious autoimmune disease, and with the development of gene sequencing in recent years, our study aims to develop a gene-based predictive model to explore the identification of SLE at the genetic level. First, gene expression datasets of SLE whole blood samples were collected from the Gene Expression Omnibus (GEO) database. After the datasets were merged, they were divided into training and validation datasets in the ratio of 7:3, where the SLE samples and healthy samples of the training dataset were 334 and 71, respectively, and the SLE samples and healthy samples of the validation dataset were 143 and 30, respectively. The training dataset was used to build the disease risk prediction model, and the validation dataset was used to verify the model identification ability. We first analyzed differentially expressed genes (DEGs) and then used Lasso and random forest (RF) to screen out six key genes (OAS3, USP18, RTP4, SPATS2L, IFI27 and OAS1), which are essential to distinguish SLE from healthy samples. With six key genes incorporated and five iterations of 10-fold cross-validation performed into the RF model, we finally determined the RF model with optimal mtry. The mean values of area under the curve (AUC) and accuracy of the models were over 0.95. The validation dataset was then used to evaluate the AUC performance and our model had an AUC of 0.948. An external validation dataset (GSE99967) with an AUC of 0.810, an accuracy of 0.836, and a sensitivity of 0.921 was used to assess the model’s performance. The external validation dataset (GSE185047) of all SLE patients yielded an SLE sensitivity of up to 0.954. The final high-throughput RF model had a mean value of AUC over 0.9, again showing good results. In conclusion, we identified key genetic biomarkers and successfully developed a novel disease risk prediction model for SLE that can be used as a new SLE disease risk prediction aid and contribute to the identification of SLE.

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“…As for axonal Charcot-Marie-Tooth disease, a cohort study from Italy showed that HSPB1 mutation account for about 4% clinical identified CMT2 patients [ 13 ]. HSPB1, as an important chaperone protein, is also closely related to a variety of other diseases, including lung cancer, colorectal cancer, diabetes, ocular diseases, coronary heart disease and atrial fibrillation [ 15 , 16 , 17 , 18 , 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Heterogeneous Clinical Phenotypes of dHMN Caused by Mutation in HSPB1 Gene: A Case Series

et al. 2022

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Mutations in HSPB1 are known to cause Charcot-Marie-Tooth disease type 2F (CMT2F) and distal hereditary motor neuropathy (dHMN). In this study, we presented three patients with mutation in HSPB1 who were diagnosed with dHMN. Proband 1 was a 14-year-old male with progressive bilateral lower limb weakness and walking difficulty for four years. Proband 2 was a 65-year-old male with chronic lower limb weakness and restless legs syndrome from the age of 51. Proband 3 was a 50-year-old female with progressive weakness, lower limbs atrophy from the age of 44. The nerve conduction studies (NCS) suggested axonal degeneration of the peripheral motor nerves and needle electromyography (EMG) revealed chronic neurogenic changes in probands. Open sural nerve biopsy for proband 2 and the mother of proband 1 showed mild to moderate loss of myelinated nerve fibers with some nerve fiber regeneration. A novel p.V97L in HSPB1 was identified in proband 3, the other two variants (p.P182A and p.R127W) in HSPB1 have been reported previously. The functional studies showed that expressing mutant p.V97L HSPB1 in SH-SY5Y cells displayed a decreased cell activity and increased apoptosis under stress condition. Our study expands the clinical phenotypic spectrum and etiological spectrum of HSPB1 mutation.

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Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease

Cited by 37 publications

References 57 publications

Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer

Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer

Establishment and analysis of a disease risk prediction model for the systemic lupus erythematosus with random forest

Heterogeneous Clinical Phenotypes of dHMN Caused by Mutation in HSPB1 Gene: A Case Series

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