SHP2: The protein tyrosine phosphatase involved in chronic pulmonary inflammation and fibrosis.
Chun-Jung ChangChiou-Feng LinBing-Chang ChenPei-Yun LinChia-Ling ChenPublished in: IUBMB life (2021)
Chronic respiratory diseases (CRDs), including pulmonary fibrosis, chronic obstructive pulmonary disease (COPD), lung cancer, and asthma, are significant global health problems due to their prevalence and rising incidence. The roles of protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs) in controlling tyrosine phosphorylation of targeting proteins modulate multiple physiological cellular responses and contribute to the pathogenesis of CRDs. Src homology-2 domain-containing PTP2 (SHP2) plays a pivotal role in modulating downstream growth factor receptor signaling and cytoplasmic PTKs, including MAPK/ERK, PI3K/AKT, and JAK/STAT pathways, to regulate cell survival and proliferation. In addition, SHP2 mutation and activation are commonly implicated in tumorigenesis. However, little is known about SHP2 in chronic pulmonary inflammation and fibrosis. This review discusses the potential involvement of SHP2 deregulation in chronic pulmonary inflammation and fibrosis, as well as the therapeutic effects of targeting SHP2 in CRDs.
Keyphrases
- signaling pathway
- pi k akt
- chronic obstructive pulmonary disease
- oxidative stress
- growth factor
- pulmonary hypertension
- global health
- cell proliferation
- lung function
- pulmonary fibrosis
- protein protein
- public health
- cell cycle arrest
- mental health
- binding protein
- cancer therapy
- amino acid
- cell death
- cystic fibrosis
- small molecule
- protein kinase
- liver fibrosis
- drug delivery