Chinese medical journal pulmonary and critical care medicine最新文献

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease with a dismal prognosis. Early diagnosis, accurate prognosis, and personalized therapeutic interventions are essential for improving patient outcomes. Biomarkers, as measurable indicators of biological processes or disease states, hold significant promise in IPF management. In recent years, there has been a growing interest in identifying and validating biomarkers for IPF, encompassing various molecular, imaging, and clinical approaches. This review provides an in-depth examination of the current landscape of IPF biomarker research, highlighting their potential applications in disease diagnosis, prognosis, and treatment response. Additionally, the challenges and future perspectives of biomarker integration into clinical practice for precision medicine in IPF are discussed.

Germline genetic variants, including single-nucleotide variants (SNVs) and copy number variants (CNVs), account for interpatient heterogeneity. In the past several decades, genome-wide association studies (GWAS) have identified multiple lung cancer-associated SNVs in Caucasian and Chinese populations. These variants either reside within coding regions and change the structure and function of cancer-related proteins or reside within non-coding regions and alter the expression level of cancer-related proteins. The variants can be used not only for cancer risk assessment and prevention but also for the development of new therapies. In this review, we discuss the lung cancer-associated SNVs identified to date, their contributions to lung tumorigenesis and prognosis, and their potential use in predicting prognosis and implementing therapeutic strategies.

Neutrophil extracellular traps (NETs), extrusions of intracellular DNA with attached granular material that exert an antibacterial effect through entangling, isolating, and immobilizing microorganisms, have been extensively studied in recent decades. The primary role of NETs is to entrap and facilitate the killing of bacteria, fungi, viruses, and parasites, preventing bacterial and fungal dissemination. NET formation has been described in many pulmonary diseases, including both infectious and non-infectious. NETs are considered a double-edged sword. As innate immune cells, neutrophils release NETs to kill pathogens and remove cellular debris. However, the deleterious effects of excessive NET release in lung disease are particularly important because NETs and by-products of NETosis can directly induce epithelial and endothelial cell death while simultaneously inducing inflammatory cytokine secretion and immune-mediated thrombosis. Thus, NET formation must be tightly regulated to preserve the anti-microbial capability of NETs while minimizing damage to the host. In this review, we summarized the recent updates on the mechanism of NETs formation and pathophysiology associated with excessive NETs, aiming to provide insights for research and treatment of pulmonary infectious diseases.

Cellular senescence is a status of irreversible growth arrest, which can be triggered by the p53/p21^cip1 and p16^INK4/Rb pathways via intrinsic and external factors. Senescent cells are typically enlarged and flattened, and characterized by numerous molecular features. The latter consists of increased surfaceome, increased residual lysosomal activity at pH 6.0 (manifested by increased activity of senescence-associated beta-galactosidase [SA-β-gal]), senescence-associated mitochondrial dysfunction, cytoplasmic chromatin fragment, nuclear lamin b1 exclusion, telomere-associated foci, and the senescence-associated secretory phenotype. These features vary depending on the stressor leading to senescence and the type of senescence. Cellular senescence plays pivotal roles in organismal aging and in the pathogenesis of aging-related diseases. Interestingly, senescence can also both promote and inhibit wound healing processes. We recently report that senescence as a programmed process contributes to normal lung development. Lung senescence is also observed in Down Syndrome, as well as in premature infants with bronchopulmonary dysplasia and in a hyperoxia-induced rodent model of this disease. Furthermore, this senescence results in neonatal lung injury. In this review, we briefly discuss the molecular features of senescence. We then focus on the emerging role of senescence in normal lung development and in the pathogenesis of bronchopulmonary dysplasia as well as putative signaling pathways driving senescence. Finally, we discuss potential therapeutic approaches targeting senescent cells to prevent perinatal lung diseases.

Lung cancer is a leading cause of cancer deaths worldwide, consisting of two major histological subtypes: small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC). In some cases, NSCLC patients may undergo a histological transformation to SCLC during clinical treatments, which is associated with resistance to targeted therapy, immunotherapy, or chemotherapy. The review provides a comprehensive analysis of SCLC transformation from NSCLC, including biological mechanism, clinical relevance, and potential treatment options after transformation, which may give a better understanding of SCLC transformation and provide support for further research to define better therapy options.

Background

Light at night (LAN) has become a concern in interdisciplinary research in recent years. This global interdisciplinary study aimed to explore the exposure–lag–response association between LAN exposure and lung cancer incidence.

Methods

LAN data were obtained from the Defense Meteorological Satellite Program's Operational Linescan System. Data of lung cancer incidence, socio-demographic index, and smoking prevalence of populations in 201 countries/territories from 1992 to 2018 were collected from the Global Burden of Disease Study. Spearman correlation tests and population-weighted linear regression analysis were used to evaluate the correlation between LAN exposure and lung cancer incidence. A distributed lag nonlinear model (DLNM) was used to assess the exposure–lag effects of LAN exposure on lung cancer incidence.

Results

The Spearman correlation coefficients were 0.286–0.355 and the population-weighted linear regression correlation coefficients were 0.361–0.527. After adjustment for socio-demographic index and smoking prevalence, the Spearman correlation coefficients were 0.264–0.357 and the population-weighted linear regression correlation coefficients were 0.346–0.497. In the DLNM, the maximum relative risk was 1.04 (1.02–1.06) at LAN exposure of 8.6 with a 2.6-year lag time. After adjustment for socio-demographic index and smoking prevalence, the maximum relative risk was 1.05 (1.02–1.07) at LAN exposure of 8.6 with a 2.4-year lag time.

Conclusion

High LAN exposure was associated with increased lung cancer incidence, and this effect had a specific lag period. Compared with traditional individual-level studies, this group-level study provides a novel paradigm of effective, efficient, and scalable screening for risk factors.