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作 者:Mahsa Zabihi Mahtab Shahriari Felordi Arun Lingampally Saverio Bellusci Xuran Chu Elie El Agha
机构地区:[1]Department of Medicine V,Internal Medicine,Infectious Diseases and Infection Control,Universities of Giessen and Marburg Lung Center(UGMLC),German Center for Lung Research(DZL),Justus-Liebig University Giessen,Giessen 35392,Germany [2]Cardio-Pulmonary Institute(CPI),Giessen 35392,Germany [3]Institute for Lung Health(ILH),Giessen 35392,Germany [4]Department of Medicine II,Internal Medicine,Pulmonary and Critical Care,Universities of Giessen and Marburg Lung Center(UGMLC),German Center for Lung Research(DZL),Justus-Liebig University Giessen,Giessen 35392,Germany [5]Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine,Vision and Brain Health),School of Pharmaceutical Science,Wenzhou Medical University,Wenzhou,Zhejiang 325035,China
出 处:《Chinese Medical Journal Pulmonary and Critical Care Medicine》2024年第3期142-150,共9页呼吸与危重症医学(英文)
基 金:B was supported by grants from the German Research Foundation(DFG;Nos.BE 4443/1-1,BE 4443/4-1,BE4443/6-1,KFO309284237345 P7 and CRC1213268555672 projects A02 and A04);German Center for Lung Research(DZL),and Excellence Cluster CardioPulmonary Institute(CPI;No.EXC2026390649896);XC acknowledges the support of the Natural Science Foundation of Zhejiang Grant(No.LQ24H210001);EEA was supported by the DFG(Nos.EL 931/5-1,EL 931/4-1,KFO309284237345 P7 and SFB CRC1213268555672 project A04),Institute for Lung Health(ILH),CPI,and DZL.
摘 要:Idiopathic pulmonary fibrosis(IPF)is characterized by accumulation of myofibroblasts(MYFs)and extracellular matrix components,which leads to severe distortion and scarring of the gas exchange units of the lung,the alveoli,and ultimately respiratory failure.Fibrosis-associated MYFs are therefore widely regarded as the culprits that compromise the architectural makeup of the lung in fibrotic disease.During the past decade,the cellular source of MYFs has been intensely investigated.The rationale for such studies is that identifying the origin of these cells might help identify novel therapeutic targets and candidates to treat IPF patients.Recent advances in basic and translational research employing lineage tracing and multi-omics approaches have helped address the identity of MYF precursors,highlight the underlying heterogeneity,and to a less extent investigate MYF fate during fibrosis resolution.In this review,we discuss the current understanding of such important aspects of MYF biology as well as recent developments in the treatment of IPF.
关 键 词:Idiopathic pulmonary fibrosis MYOFIBROBLASTS Fibrotic disease Myofibroblast heterogeneity Lineage tracing
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