Colorectal cancer remains one of the leading causes of morbidity and mortality worldwide.Despite notable advances in early detection and therapeutic strategies,the molecular mechanisms underlying tumor survival,chemot...Colorectal cancer remains one of the leading causes of morbidity and mortality worldwide.Despite notable advances in early detection and therapeutic strategies,the molecular mechanisms underlying tumor survival,chemotherapy resistance,and metastasis are not yet fully understood.MicroRNAs(miRNAs)have emerged as pivotal regulators of cancer development,as they modulate gene expression and orchestrate key signaling pathways.However,the epigenetic mechanisms that control miRNA expression and their downstream gene targets remain largely unclear.In this review,we highlight the critical role of the colorectal cancer microenvironment in influencing miRNA expression and discuss how this regulation contributes to tumorigenesis.A better understanding of these processes may lead to the identification of novel therapeutic targets and strategies to prevent recurrence.展开更多
Acute myocardial infarction(AMI)remains a leading global cause of morbidity and mortality,with high risk of recurrent adverse cardiovascular events.Conventional diagnostic markers often lack the sensitivity needed for...Acute myocardial infarction(AMI)remains a leading global cause of morbidity and mortality,with high risk of recurrent adverse cardiovascular events.Conventional diagnostic markers often lack the sensitivity needed for early detection and prognostic stratification.Recent advances highlight the role of microRNAs(miRNAs)and their genetic polymorphisms in regulating inflammation,fibrosis,and endothelial function in atherosclerotic disease.This review summarizes evidence on circulating miRNA expression and miRNA-related single nucleotide polymorphisms as biomarkers in AMI.Literature from PubMed,Scopus,and Web of Science was evaluated,focusing on pathways involving NF-κB,interleukin-1 receptor/toll-like receptors,and JAK/STAT signaling.Circulating miRNAs such as miR-150,miR-208,miR-26a,and miR-483-5p demonstrate strong diagnostic accuracy,while polymorphisms,particularly rs2910164 in miR-146a,are consistently associated with AMI susceptibility and adverse outcomes.These findings suggest that miRNAs and their variants may serve as non-invasive tools for diagnosis and risk prediction,supporting future integration into precision cardiovascular medicine.展开更多
Severe acute respiratory coronavirus-2(SARS-CoV-2)infection course differs between the young and healthy and the elderly with co-morbidities.In the latter a potentially lethal coronavirus disease 2019(COVID-19)cytokin...Severe acute respiratory coronavirus-2(SARS-CoV-2)infection course differs between the young and healthy and the elderly with co-morbidities.In the latter a potentially lethal coronavirus disease 2019(COVID-19)cytokine storm has been described with an unrestrained renin-angiotensin(Ang)system(RAS).RAS inhibitors[Ang converting enzyme inhibitors and Ang II type 1 receptor(AT1R)blockers]while appearing appropriate in COVID-19,display enigmatic effects ranging from protection to harm.MicroRNA-155(miR-155)-induced translational repression of key cardiovascular(CV)genes(i.e.,AT1R)restrains SARS-CoV-2-engendered RAS hyperactivity to tolerable and SARS-CoV-2-protective CV phenotypes supporting a protective erythropoietin(EPO)evolutionary landscape.MiR-155’s disrupted repression of the AT1R 1166C-allele associates with adverse CV and COVID-19 outcomes,confirming its decisive role in RAS modulation.RAS inhibition disrupts this miR-155-EPO network by further lowering EPO and miR-155 in COVID-19 with co-morbidities,thereby allowing unimpeded RAS hyperactivity to progress precariously.Current pharmacological interventions in COVID-19 employing RAS inhibition should consider these complex but potentially detrimental miR-155/EPO-related effects.展开更多
文摘Colorectal cancer remains one of the leading causes of morbidity and mortality worldwide.Despite notable advances in early detection and therapeutic strategies,the molecular mechanisms underlying tumor survival,chemotherapy resistance,and metastasis are not yet fully understood.MicroRNAs(miRNAs)have emerged as pivotal regulators of cancer development,as they modulate gene expression and orchestrate key signaling pathways.However,the epigenetic mechanisms that control miRNA expression and their downstream gene targets remain largely unclear.In this review,we highlight the critical role of the colorectal cancer microenvironment in influencing miRNA expression and discuss how this regulation contributes to tumorigenesis.A better understanding of these processes may lead to the identification of novel therapeutic targets and strategies to prevent recurrence.
文摘Acute myocardial infarction(AMI)remains a leading global cause of morbidity and mortality,with high risk of recurrent adverse cardiovascular events.Conventional diagnostic markers often lack the sensitivity needed for early detection and prognostic stratification.Recent advances highlight the role of microRNAs(miRNAs)and their genetic polymorphisms in regulating inflammation,fibrosis,and endothelial function in atherosclerotic disease.This review summarizes evidence on circulating miRNA expression and miRNA-related single nucleotide polymorphisms as biomarkers in AMI.Literature from PubMed,Scopus,and Web of Science was evaluated,focusing on pathways involving NF-κB,interleukin-1 receptor/toll-like receptors,and JAK/STAT signaling.Circulating miRNAs such as miR-150,miR-208,miR-26a,and miR-483-5p demonstrate strong diagnostic accuracy,while polymorphisms,particularly rs2910164 in miR-146a,are consistently associated with AMI susceptibility and adverse outcomes.These findings suggest that miRNAs and their variants may serve as non-invasive tools for diagnosis and risk prediction,supporting future integration into precision cardiovascular medicine.
文摘Severe acute respiratory coronavirus-2(SARS-CoV-2)infection course differs between the young and healthy and the elderly with co-morbidities.In the latter a potentially lethal coronavirus disease 2019(COVID-19)cytokine storm has been described with an unrestrained renin-angiotensin(Ang)system(RAS).RAS inhibitors[Ang converting enzyme inhibitors and Ang II type 1 receptor(AT1R)blockers]while appearing appropriate in COVID-19,display enigmatic effects ranging from protection to harm.MicroRNA-155(miR-155)-induced translational repression of key cardiovascular(CV)genes(i.e.,AT1R)restrains SARS-CoV-2-engendered RAS hyperactivity to tolerable and SARS-CoV-2-protective CV phenotypes supporting a protective erythropoietin(EPO)evolutionary landscape.MiR-155’s disrupted repression of the AT1R 1166C-allele associates with adverse CV and COVID-19 outcomes,confirming its decisive role in RAS modulation.RAS inhibition disrupts this miR-155-EPO network by further lowering EPO and miR-155 in COVID-19 with co-morbidities,thereby allowing unimpeded RAS hyperactivity to progress precariously.Current pharmacological interventions in COVID-19 employing RAS inhibition should consider these complex but potentially detrimental miR-155/EPO-related effects.
