Cardiovasc Drugs Ther
December 2024
Objective: Cardiovascular diseases (CVDs) are major public health problems that threaten the lives and health of individuals. The article has reviewed recent progresses about ferroptosis and ferroptosis-related intervention approaches for the treatment of CVDs and provided more references and strategies for targeting ferroptosis to prevent and treat CVDs.
Methods: A comprehensive review was conducted using the literature researches.
Cardiac hypertrophy results from the heart reacting and adapting to various pathological stimuli and its persistent development is a major contributing factor to heart failure. However, the molecular mechanisms of cardiac hypertrophy remain unclear. Small GTPases in the Ras, Rho, Rab, Arf and Ran subfamilies exhibit GTPase activity and play crucial roles in regulating various cellular responses.
View Article and Find Full Text PDFKelch-like ECH-associated protein 1 (KEAP1), as a negative regulator of nuclear factor erythroid 2 like 2 ( NRF2), plays a pivotal role in NRF2 signaling pathway and involves in tumorigenesis. Polymorphisms and methylation in gene promoter region may influence its expression and be related to cancer susceptibility. In this study, we examined the effect of the KEAP1-NRF2 interaction on the risk of colorectal cancer (CRC).
View Article and Find Full Text PDFLong noncoding RNAs (lncRNA) are emerging as a novel class of regulators in gene expression associated with tumorigenesis. However, the role of lncRNAs in papillary thyroid carcinoma (PTC) is poorly understood. Here, we conducted global lncRNA profiling and identified lncRNA AB074169 (lncAB) as significantly downregulated in PTC.
View Article and Find Full Text PDFmiR-17-92 cluster is identified as a potential oncogenic miRNA. The aim of this study was to investigate the association of polymorphisms in the promoter region of miR-17-92 cluster with the risk of colorectal cancer (CRC). Three polymorphisms (i.
View Article and Find Full Text PDFAim: IL-27 has potent antitumor effects. We aimed to examine the contribution of single nucleotide polymorphisms in IL-27 to the risk of papillary thyroid carcinoma (PTC).
Materials & Methods: IL-27 rs153109 and rs17855750 were analyzed in 496 PTC patients and 629 controls, using a polymerase chain reaction-restriction fragment length polymorphism method.
The aim of this study was to investigate the effect of a polymorphism rs4705341 in the flanking region of miR-143/145 on the risk of colorectal cancer (CRC). The rs4705341 polymorphism was analyzed in 1002 cases and 1062 controls using a polymerase chain reaction-restriction fragment length polymorphism method. We found a significantly reduced CRC susceptibility with miR-143/145 rs4705341 in homozygote comparison (adjusted OR = 0.
View Article and Find Full Text PDFMiR-143/145 is down-regulated in cervical cancer, which may serve as a tumor suppressor by targeting KRAS and Ras-responsive element-binding protein (RREB1). Activated KRAS leads to down-regulation of miR-143/145 transcription in a RREB1-dependent manner, establishing a miR-143/145-KRAS-RREB1 feedback loop. A polymorphism rs4705343C/T in the promoter of miR-143/145 might influence the binding of TATA-binding protein.
View Article and Find Full Text PDFBackground: Toxoplasma gondii is an obligate, intracellular protozoan that infects almost all warm-blooded animals, including humans, domesticated and wild animals. Recent studies of Toxoplasma gondii isolates from animals in different regions of China have shown a limited genetic diversity with the dominance of the ToxoDB PCR-RFLP genotype #9 named as "Chinese 1". However, there is not much published information regarding its prevalence in domestic animals from Guizhou province, a subtropical region in Southwest China.
View Article and Find Full Text PDFKRAS mutation is frequently detected in a series of cancers, including papillary thyroid cancer (PTC). Recently, a genetic variant of rs712 in the 3' untranslated region of the KRAS gene has been reported to be functional in the regulation of KRAS by disrupting complementary site of let-7 and miR-181. We aimed to investigate whether the polymorphism is a risk factor for PTC.
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