摘要
Asthma affects about 300 million people worldwide, placing an enormous strain on health resources inmany countries. Evidence is increasing that asthma is a complex condition with different underlying pathophysiologiesJ Scientists around the world have devoted much effort to unveiling this heterogeneity, from phenotyping initially focused on combinations of clinical characteristics, towards endotypes evolving which link pathophysiological mechanism to subtypes of asthma.2 The identification of these endotypes, either by matching biology, genetics and therapeutic responses with clinically defined phenotypes or through unbiased genomic approaches, remains limited.3 Moving forward, ongoing studies that expand on these insights into the molecular signatures should enhance our ability to define the endotypes and lead to more targeted approaches to asthma therapy.4
Asthma affects about 300 million people worldwide, placing an enormous strain on health resources inmany countries. Evidence is increasing that asthma is a complex condition with different underlying pathophysiologiesJ Scientists around the world have devoted much effort to unveiling this heterogeneity, from phenotyping initially focused on combinations of clinical characteristics, towards endotypes evolving which link pathophysiological mechanism to subtypes of asthma.2 The identification of these endotypes, either by matching biology, genetics and therapeutic responses with clinically defined phenotypes or through unbiased genomic approaches, remains limited.3 Moving forward, ongoing studies that expand on these insights into the molecular signatures should enhance our ability to define the endotypes and lead to more targeted approaches to asthma therapy.4
基金
This work was supported by agrant from the National Natural Science Foundation of China(No.30900648)