期刊
ANNUAL REVIEW OF MEDICINE
卷 55, 期 -, 页码 395-417出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.med.55.091902.103810
关键词
inflammation; regeneration; fibroblasts; cell differentiation; apoptosis
资金
- NHLBI NIH HHS [HL-67967, P50 HL-056402] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL067967, P50HL056402] Funding Source: NIH RePORTER
Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of pulmonary fibrosis as a dysregulated repair process that is perpetually turned on even though classical inflammatory pathways may be dampened or switched off. Significant regional heterogeneity, with varied histopathological patterns of inflammation and fibrosis, has been observed in individual patients with idiopathic pulmonary fibrosis. We discuss environmental factors and host response factors, such as genetic susceptibility and age, that may influence these varied manifestations. Better understanding of the mechanisms of lung repair, which include alveolar reepithelialization, myofibroblast differentiation/activation, and apoptosis, should offer more effective therapeutic options for progressive pulmonary fibrosis.
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