Liposomes carrying MBD2 siRNA protect mice against BLM-induced lung injury and fibrosis by targeting macrophage M2 program.

Idiopathic pulmonary fibrosis (IPF) has been extensively studied in recent decades due to its rising incidence and high mortality. Despite an abundance of research, the mechanisms, immune-associated mechanisms, of IPF are poorly understood. While defining immunopathogenic mechanisms as the primary pathogenesis is controversial, recent studies have verified the contribution of the immune system to the fibrotic progression of IPF. Extensive evidence has shown the potential role of T cells in fibrotic progression. In this review, we emphasize the features of T cells in IPF and highlight the controversial roles of different subtypes of T cells or even two distinct effects of one type of T-cell in diverse settings, and multiple chemokines and cell products are discussed. Furthermore, we discuss the potential development of treatments targeting the immune molecules of T cells and the feasibility of immune therapies for IPF in clinical practice.

Idiopathic pulmonary fibrosis (IPF) is a progressive and life-threatening interstitial lung disease characterized by excessive extracellular matrix deposition and fibroblast activation. Emerging evidence suggests that amino acid metabolism plays a crucial role in the pathogenesis of pulmonary fibrosis. Key amino acids, including arginine, proline, and glutamine, contribute to the regulation of fibroblast activity and collagen synthesis, all of which are essential for fibrotic progression. Studies in experimental models of pulmonary fibrosis have demonstrated significant metabolic dysregulation, further highlighting its relevance in disease development. Moreover, targeting amino acid metabolism has emerged as a promising therapeutic strategy, with novel drugs and interventions designed to modulate metabolic pathways showing potential in preclinical and clinical studies. This review explores the intricate interplay between amino acid metabolism and pulmonary fibrosis, discusses its implications for disease progression, and evaluates the therapeutic prospects of metabolic interventions in IPF management. Understanding these metabolic mechanisms may pave the way for more effective and personalized treatment strategies for IPF.

Background: Chronic obstructive pulmonary disease (COPD) characterized by the airway and lung inflammation, is a leading cause of morbidity and mortality worldwide, especially among smokers over 40 years of age and individuals exposed to biomass smoke. Although the detailed mechanisms of this disease remain elusive, there is feasible evidence that protein posttranslational modifications (PTMs) may play a role in its pathoetiology. We thus conducted studies to dissect the effect of cigarette smoke extracts (CSE) on the change of SUMOylated substrates in human bronchial epithelial cells (HBEs). Methods: Samples were collected in HBEs with or without 24 h of CSE insult and then subjected to Western-blot and LC-MS/MS analysis. Subsequently, bioinformatic tools were used to analyze the data. The effect of SUMOylation on cytochrome P450 1A1 (CYP1A1) was evaluated by flow cytometry. Results: It was noted that CSE stimulated HBEs to undergo a SUMOylation turnover as evidenced by the changes of SUMOylated substrates and SUMOylation levels for a particular substrate. The SUMOylated proteins are relevant to the regulation of biological processes, molecular function and cellular components. Particularly, CSE stimulated a significant increase of SUMOylated CYP1A1, a critical enzyme involved in the induction of oxidative stress. Conclusions: Our data provide a protein SUMOylation profile for better understanding of the mechanisms underlying COPD and support that smoking induces oxidative stress in HBEs, which may predispose to the development of COPD in clinical settings.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic lung disease with limited treatment options and efficacy. Evidence suggests that IPF arises from genetic, environmental, and aging-related factors. The pathogenic mechanisms of IPF primarily involve dysregulated repeated microinjuries to epithelial cells, abnormal fibroblast/myofibroblast activation, and extracellular matrix (ECM) deposition, but thus far, the exact etiology remains unclear. Noncoding RNAs (ncRNAs) play regulatory roles in various biological processes and have been implicated in the pathophysiology of multiple fibrotic diseases, including IPF. This review summarizes the roles of ncRNAs in the pathogenesis of IPF and their potential as diagnostic and therapeutic targets.