Abstract
Asthma is a chronic airway inflammatory disorder related to variable expiratory airflow limitation, leading to wheeze, shortness of breath, chest tightness, and cough. Its characteristic features include airway inflammation, airway remodeling and airway hyperresponsiveness. The pathogenesis of asthma remains extremely complicated and the detailed mechanisms are not clarified. Long noncoding RNAs (lncRNAs) have been reported to play a prominent role in asthma and function as modulators of various aspects in pathological progress of asthma. Here, we summarize recent advances of lncRNAs in asthma pathogenesis to guide future researches, clinical treatment and drug development, including their regulatory functions in the T helper (Th) 1/Th2 imbalance, Th17/T regulatory (Treg) imbalance, eosinophils dysfunction, macrophage polarization, airway smooth muscle cells proliferation, and glucocorticoid insensitivity.
Highlights
Asthma is a common pulmonary disease, featured by airway inflammatory response, airway hyperresponsiveness (AHR), and airway remodeling
We review established literature on Long noncoding RNAs (lncRNAs) in asthma (Table 1) and discuss their regulation of T helper (Th) 1/Th2 imbalance, Th17/T regulatory (Treg) imbalance, EOS dysfunction, macrophage polarization, airway smooth muscle cells (ASMCs) proliferation and glucocorticoid insensitivity to further clarify the specific mechanisms of lncRNAs in asthma pathogenesis (Figure 3)
We find that there is no research to discuss the relationship between lncRNAs and Th22, Th9, Th25, or T follicular helper cells, which can be the focus of future research
Summary
Asthma is a common pulmonary disease, featured by airway inflammatory response, airway hyperresponsiveness (AHR), and airway remodeling. LncRNAs are non-protein coding transcripts with a length of at least 200 nucleotides (Hung and Chang, 2010) and are generally classified into antisense lncRNAs, pseudogenes lncRNAs, intronic lncRNAs, and intergenic lncRNAs by protein-coding gene sequences and position (Booton and Lindsay, 2014) Referring to their classical mechanisms, they can regulate genes (translation inhibition, splicing modification, and mRNA degradation) via the direct bond to the genes and sponge the microRNA (miR) as a competitive endogenous RNA (ceRNA) to prevent. They form chromatin remodeling complexes to modulate ubiquitination and methylation They are as similar to DNA, which can function as an RNA decoy that binds to the transcription factors to regulate their activity and downstream signaling pathways. We review established literature on lncRNAs in asthma (Table 1) and discuss their regulation of T helper (Th) 1/Th2 imbalance, Th17/T regulatory (Treg) imbalance, EOS dysfunction, macrophage polarization, airway smooth muscle cells (ASMCs) proliferation and glucocorticoid insensitivity to further clarify the specific mechanisms of lncRNAs in asthma pathogenesis (Figure 3)
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