Cigarette smoke-induced galectin-3 as a diagnostic biomarker and therapeutic target in lung tissue remodeling

• Published in: Life sciences (1973) 2024-02, Vol.339, p.122433-122433, Article 122433
• Main Authors: Sharma, Jiten R., Dubey, Anupama, Yadav, Umesh C.S.
• Format: Article
• Language: English
• Subjects: Biomarkers - metabolism; Cigarette smoke; Cigarette Smoking; COPD; Galectin 3 - metabolism; Galectin-3; Humans; Lung - metabolism; Lung cancer; Lung tissue remodeling; Oxidative stress; Pharmacological strategies; Pulmonary Disease, Chronic Obstructive - diagnosis; Pulmonary Disease, Chronic Obstructive - etiology; Pulmonary Disease, Chronic Obstructive - metabolism; Tobacco Products
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2024.122433

Galectin-3 (Gal-3), a multifunctional carbohydrate-binding lectin, has emerged as a key player in various biological processes including inflammation, cancer, cardiovascular diseases and fibrotic disorders, however it remains unclear if Gal-3 is a bystander or drives lung tissue remodeling (LTR). Persistent exposure to cigarette smoke (CS) is the leading cause of oxidative and inflammatory damage to the lung tissues. CS-induced pathological increase in Gal-3 expression has been implicated in the pathogenesis of various respiratory conditions, such as chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and lung cancer. We and others have reported that CS induces Gal-3 synthesis and secretion, which modulates the pathological signaling pathways in lung epithelial cells implicating Gal-3 as a novel diagnostic marker and a factor driving LTR in CS-exposed lungs. Therefore, pharmacological interventions targeting Gal-3 and its upstream and downstream signaling pathways can help combat CS-induced LTR. Excitingly, preclinical models have demonstrated the efficacy of interventions such as Gal-3 expression inhibition, Gal-3 receptor blockade, and signaling pathways modulation open up promising avenues for future therapeutic interventions. Furthermore, targeting extracellular vesicles-mediated Gal-3 release and the potential of microRNA-based therapy are emerging as novel therapeutic approaches in CS-induced LTR and have been discussed in this article. [Display omitted] •Cigarette smoking (CS)-induced oxidative stress causes elevated level of Galectin-3 (Gal-3) in the lungs.•Gal-3, a multifunctional carbohydrate-binding lectin, is involved in inflammation, tissue remodeling, and fibrosis.•Gal-3 regulates epithelial-mesenchymal transition (EMT), an evolutionarily conserved physiological and pathological process.•Gal-3 mediates lung tissue remodeling (LTR) in COPD via various mechanisms and pathways.•Pharmacological intervention targeting Gal-3 synthesis and secretion can combat CS-induced LTR by regulating EMT.