2020
Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation
Gu SX, Tyagi T, Jain K, Gu VW, Lee SH, Hwa JM, Kwan JM, Krause DS, Lee AI, Halene S, Martin KA, Chun HJ, Hwa J. Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation. Nature Reviews Cardiology 2020, 18: 194-209. PMID: 33214651, PMCID: PMC7675396, DOI: 10.1038/s41569-020-00469-1.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAdministration, InhalationAnticoagulantsBlood Coagulation DisordersBlood Platelet DisordersCOVID-19COVID-19 Drug TreatmentEndothelium, VascularEndothelium-Dependent Relaxing FactorsEpoprostenolHeart Disease Risk FactorsHumansIloprostInflammationNitric OxidePlatelet Aggregation InhibitorsSARS-CoV-2Systemic Inflammatory Response SyndromeThrombosisThrombotic MicroangiopathiesVascular DiseasesVasodilator AgentsVenous ThromboembolismConceptsCardiovascular risk factorsRisk factorsCOVID-19Severe acute respiratory syndrome coronavirus 2Pre-existing cardiovascular diseaseAcute respiratory syndrome coronavirus 2Traditional cardiovascular risk factorsAcute respiratory distress syndromeRespiratory syndrome coronavirus 2Respiratory distress syndromeManagement of patientsSyndrome coronavirus 2COVID-19 pathologyCoronavirus disease 2019Potential therapeutic strategyCytokine stormEndothelial dysfunctionThrombotic complicationsDistress syndromeExcessive inflammationCoronavirus 2Severe outcomesAdvanced ageCardiovascular diseaseDisease 2019
2018
Genome-Wide Expression Analysis Suggests Hypoxia-Triggered Hyper-Coagulation Leading to Venous Thrombosis at High Altitude
Jha PK, Sahu A, Prabhakar A, Tyagi T, Chatterjee T, Arvind P, Nair J, Gupta N, Kumari B, Nair V, Bajaj N, Shanker J, Sharma M, Kumar B, Ashraf MZ. Genome-Wide Expression Analysis Suggests Hypoxia-Triggered Hyper-Coagulation Leading to Venous Thrombosis at High Altitude. Thrombosis And Haemostasis 2018, 118: 1279-1295. PMID: 29864786, DOI: 10.1055/s-0038-1657770.Peer-Reviewed Original ResearchMeSH KeywordsAdultAltitudeBlood CoagulationBlood Coagulation DisordersCase-Control StudiesGene Expression ProfilingGene Regulatory NetworksGene-Environment InteractionGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansHypoxiaMalePhenotypeRisk AssessmentRisk FactorsTranscriptomeVenous ThrombosisConceptsDeep vein thrombosisGenome-wide expression analysisDifferential expressionVenous thromboembolismEnrichment of genesGenes/pathwaysGene expression profilesHypoxia-responsive genesGene expression profilingRisk factorsGene OntologyOnset of VTEBioinformatics analysisExpression analysisExpression profilingExpression profilesPathway analysisMolecular mechanismsAdditional risk factorsQuantitative reverse transcription polymerase chain reactionReverse transcription-polymerase chain reactionPathophysiology of DVTCommon cardiovascular diseaseRelevant pathwaysGenes
2017
Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia
Gupta N, Sahu A, Prabhakar A, Chatterjee T, Tyagi T, Kumari B, Khan N, Nair V, Bajaj N, Sharma M, Ashraf MZ. Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: 4763-4768. PMID: 28420787, PMCID: PMC5422823, DOI: 10.1073/pnas.1620458114.Peer-Reviewed Original ResearchConceptsExpression of NLRP3Venous thrombosisVenous thromboembolismIL-1βCaspase-1Activation of NLRP3Acute thrombotic eventsHypoxic conditionsIL-1β secretionNLRP3 inflammasome complexHypoxia-inducible factorThromboembolic eventsProinflammatory stateSystemic hypoxiaThrombotic eventsPreclinical findingsAltered hemostasisRisk factorsCardiovascular conditionsCommon causeInflammasome activationThrombosisHealthy individualsPyrin domainHIF-1α