Pengwei Ren, PhD
Associate Research ScientistCards
About
Research
Publications
2023
Everolimus combined with PD-1 blockade inhibits progression of triple-negative breast cancer
Li G, Hu J, Cho C, Cui J, Li A, Ren P, Zhou J, Wei W, Zhang T, Liu X, Liu W. Everolimus combined with PD-1 blockade inhibits progression of triple-negative breast cancer. Cellular Signalling 2023, 109: 110729. PMID: 37257766, DOI: 10.1016/j.cellsig.2023.110729.Peer-Reviewed Original ResearchConceptsT cell tumor infiltrationTriple-negative breast cancerCD8+ T cell tumor infiltrationBreast cancerTumor infiltrationLack of target receptorsAnti-PD-1 antibodyAggressive subtype of breast cancerModels of triple-negative breast cancerSubtypes of breast cancerPD-L1 expressionEstrogen-positive breast cancerMTOR inhibitor everolimusPositive breast cancerProgression of triple-negative breast cancerReduced tumor growthAvailable treatment optionsCombination treatment strategiesPromote cancer cell survivalTreatment of estrogen-positive breast cancerAttenuate tumor progressionNonspecific cytotoxic agentsCancer cell survivalVascular endothelial cellsPotential therapeutic strategyFN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome
Chen M, Cavinato C, Hansen J, Tanaka K, Ren P, Hassab A, Li D, Youshao E, Tellides G, Iyengar R, Humphrey J, Schwartz M. FN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome. Arteriosclerosis Thrombosis And Vascular Biology 2023, 43: e132-e150. PMID: 36994727, PMCID: PMC10133209, DOI: 10.1161/atvbaha.123.319120.Peer-Reviewed Original ResearchConceptsContractile gene expressionSmooth muscle cellsGene expressionMgR miceWild-type smooth muscle cellsMarfan miceAortic aneurysmMouse modelMarfan syndromeMouse aortic smooth muscle cellsPathogenesis of TAACytoplasmic domainVascular smooth muscle cellsThoracic aortic aneurysmAortic smooth muscle cellsCultured smooth muscle cellsNF-kB activationNF-kB inhibitionMolecular mechanismsIntegrin α2ECM remodelingElastic fiber integrityPhenotypic modulationMarfan's aneurysmsMgR/Hedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells
Jiang B, Wang S, Song G, Jiang Q, Fan M, Fang C, Li X, Soh C, Manes T, Cheru N, Qin L, Ren P, Jortner B, Wang Q, Quaranta E, Yoo P, Geirsson A, Davis R, Tellides G, Pober J, Jane-Wit D. Hedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells. Science Signaling 2023, 16: eabo3406. PMID: 36943921, PMCID: PMC10061549, DOI: 10.1126/scisignal.abo3406.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryChronic vascular inflammationT cellsNLRP3 inflammasomeVascular inflammationChronic inflammationEndothelial cellsIFN-γ responsesControl T cellsNLRP3 inflammasome activityT memory cellsAllograft vasculopathyVascular sequelaeHuman endothelial cellsCoronary arteryEffector responsesCell-autonomous roleInflammasome activityMouse modelInflammationPatient samplesVigorous recruitmentInflammasomePrimary human cellsImmune signalingLonafarnib improves cardiovascular function and survival in a mouse model of Hutchinson-Gilford progeria syndrome
Murtada S, Mikush N, Wang M, Ren P, Kawamura Y, Ramachandra A, Li D, Braddock D, Tellides G, Gordon L, Humphrey J. Lonafarnib improves cardiovascular function and survival in a mouse model of Hutchinson-Gilford progeria syndrome. ELife 2023, 12: e82728. PMID: 36930696, PMCID: PMC10023154, DOI: 10.7554/elife.82728.Peer-Reviewed Original ResearchConceptsMouse modelLeft ventricular diastolic functionHutchinson-Gilford progeria syndromeVentricular diastolic functionPulse wave velocityDrug-associated effectsMTOR inhibitor rapamycinCardiovascular sequelaeDiastolic functionProgeria syndromeDevastating conditionCardiac functionCardiovascular functionClinical trialsCardiovascular diseaseMuscular arteriesUS FoodDrug AdministrationProgeria miceArterial structurePremature deathLonafarnibCardiovascular structureCharacteristics of agingInhibitor rapamycinTrehalose attenuates abdominal aortic aneurysm formation by inducing autophagy in smooth muscle cells.
Jiang B, Li X, Wang M, Li G, Ren P, Wang Y, Xin S, Qin L. Trehalose attenuates abdominal aortic aneurysm formation by inducing autophagy in smooth muscle cells. Journal Of Geriatric Cardiology 2023, 20: 214-222. PMID: 37091261, PMCID: PMC10114191, DOI: 10.26599/1671-5411.2023.03.002.Peer-Reviewed Original ResearchElastase-induced abdominal aortic aneurysmContractile phenotypeAbdominal aortic aneurysm (AAAGieson stainingVehicle-treated miceMeasuring aortic diameterAbdominal aortic aneurysm formationAortic aneurysm formationAbdominal aortic aneurysmTrehalose-treated groupSmooth muscle cellsExpression of autophagy markersVerhoeff-Van Gieson stainSmooth muscle cell contractile phenotypeAutophagy inducerAorta dilatationAortic diameterLeukocyte infiltrationAortic aneurysmVascular histologyDecreased inflammationAAA progressionMouse modelAbdominal aortaMuscle cells
2022
mTOR inhibition prevents angiotensin II–induced aortic rupture and pseudoaneurysm but promotes dissection in Apoe-deficient mice
He C, Jiang B, Wang M, Ren P, Murtada SI, Caulk AW, Li G, Qin L, Assi R, Lovoulos CJ, Schwartz MA, Humphrey JD, Tellides G. mTOR inhibition prevents angiotensin II–induced aortic rupture and pseudoaneurysm but promotes dissection in Apoe-deficient mice. JCI Insight 2022, 7: e155815. PMID: 35132962, PMCID: PMC8855820, DOI: 10.1172/jci.insight.155815.Peer-Reviewed Original ResearchConceptsApoE-deficient miceAngiotensin IIVascular wall cellsAortic tearAortic ruptureMTOR inhibitionSmooth muscle cell hypertrophyMatricellular proteinWall cellsSuprarenal abdominal aortaMuscle cell hypertrophyExtracellular matrix accumulationInhibition of mTORRole of mTORSubadventitial hematomaFree ruptureAortic dissectionAortic diseaseAortic aneurysmSignificant dissectionAbdominal aortaHemorrhagic lesionsExtensive dissectionMetalloproteinase expressionCell hypertrophy
2021
Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in mice
Spronck B, Latorre M, Wang M, Mehta S, Caulk AW, Ren P, Ramachandra AB, Murtada SI, Rojas A, He CS, Jiang B, Bersi MR, Tellides G, Humphrey JD. Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in mice. Journal Of The Royal Society Interface 2021, 18: 20210336. PMID: 34314650, PMCID: PMC8315831, DOI: 10.1098/rsif.2021.0336.Peer-Reviewed Original ResearchConceptsAortic remodellingWall stressAngiotensin II infusionInflammatory cell infiltrationC57BL/6 J miceSmooth muscle contractile processHigh wall stressVasoconstrictive capacityII infusionBlood pressureInflammatory cellsCell infiltrationMean wall stressJ miceThoracic aortaMaladaptive remodellingImmune processesAortaBulk RNA sequencingBiomechanical assessmentAdaptive remodellingContractile processMarked increaseRemodellingVasoconstriction