Environmental Causes of Idiopathic Pulmonary Fibrosis

Gandhi, Sheiphali; Tonelli, Roberto; Murray, Margaret; Samarelli, Anna Valeria; Spagnolo, Paolo

doi:10.3390/ijms242216481

Cited by 5 publications

(2 citation statements)

References 109 publications

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“…However, the etiology of metabolic mechanisms, such as the formation of LLMs in PF, remains incompletely understood. Like COPD, the inhalation of noxious particles such as CS, dust, and silica is considered a critical environmental factor contributing to PF pathogenesis [ 125 , 126 , 127 ]. As the first line of defense of the pulmonary immune system, AMs are actively enrolled in maintaining lipid homeostasis.…”

Section: Llms In Pfmentioning

confidence: 99%

Lipid-Laden Macrophages in Pulmonary Diseases

Zhu,

Choi,

Somanath

et al. 2024

Cells

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Pulmonary surfactants play a crucial role in managing lung lipid metabolism, and dysregulation of this process is evident in various lung diseases. Alternations in lipid metabolism lead to pulmonary surfactant damage, resulting in hyperlipidemia in response to lung injury. Lung macrophages are responsible for recycling damaged lipid droplets to maintain lipid homeostasis. The inflammatory response triggered by external stimuli such as cigarette smoke, bleomycin, and bacteria can interfere with this process, resulting in the formation of lipid-laden macrophages (LLMs), also known as foamy macrophages. Recent studies have highlighted the potential significance of LLM formation in a range of pulmonary diseases. Furthermore, growing evidence suggests that LLMs are present in patients suffering from various pulmonary conditions. In this review, we summarize the essential metabolic and signaling pathways driving the LLM formation in chronic obstructive pulmonary disease, pulmonary fibrosis, tuberculosis, and acute lung injury.

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Section: Llms In Pfmentioning

confidence: 99%

Lipid-Laden Macrophages in Pulmonary Diseases

Zhu,

Choi,

Somanath

et al. 2024

Cells

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“…Cigarette smoking (CS) is a lifestyle factor that can potentially be modified, which consistently ranks as one of the primary risk factors for IPF. Therefore, CS have garnered significant attention as promising areas of intervention in efforts to prevent the risk of IPF and halt its progression [4]. However, research on the specific role of smoking in driving disease progression in individuals with IPF is still limited.…”

Section: Introductionmentioning

confidence: 99%

Genetic association between smoking and DLCO in idiopathic pulmonary fibrosis patients

Yuan,

Lei,

Xing

et al. 2024

BMC Pulm Med

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Background Observational studies have shown that smoking is related to the diffusing capacity of the lungs for carbon monoxide (DLCO) in individuals with idiopathic pulmonary fibrosis (IPF). Nevertheless, further investigation is needed to determine the causal effect between these two variables. Therefore, we conducted a study to investigate the causal relationship between smoking and DLCO in IPF patients using two-sample Mendelian randomization (MR) analysis. Methods Large-scale genome-wide association study (GWAS) datasets from individuals of European descent were analysed. These datasets included published lifetime smoking index (LSI) data for 462,690 participants and DLCO data for 975 IPF patients. The inverse-variance weighting (IVW) method was the main method used in our analysis. Sensitivity analyses were performed by MR‒Egger regression, Cochran’s Q test, the leave-one-out test and the MR-PRESSO global test. Results A genetically predicted increase in LSI was associated with a decrease in DLCO in IPF patients [ORIVW = 0.54; 95% CI 0.32–0.93; P = 0.02]. Conclusions Our study suggested that smoking is associated with a decrease in DLCO. Patients diagnosed with IPF should adopt an active and healthy lifestyle, especially by quitting smoking, which may be effective at slowing the progression of IPF.

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Novel therapeutic strategies and drugs for idiopathic pulmonary fibrosis

Shi,

Zhou,

Zhai

et al. 2024

Archiv der Pharmazie

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Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease of unknown etiology. Currently, drugs used to treat IPF in clinical practice exhibit severe side effects and limitations. To address these issues, this paper discusses the therapeutic effects of preclinical targeted drugs (such as STAT3 and TGF‐β/Smad pathway inhibitors, chitinase inhibitors, PI3K and phosphodiesterase inhibitors, etc.) and natural products on IPF. Through a summary of current research progress, it is found that natural products possess multitarget effects, stable therapeutic efficacy, low side effects, and nondrug dependence. Furthermore, we discuss the significant prospects of natural product molecules in combating fibrosis by influencing the immune system, expecting that current analytical data will aid in the development of new drugs or the investigation of active ingredients in natural products for potential IPF treatments in the future.

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Environmental Causes of Idiopathic Pulmonary Fibrosis

Cited by 5 publications

References 109 publications

Lipid-Laden Macrophages in Pulmonary Diseases

Lipid-Laden Macrophages in Pulmonary Diseases

Genetic association between smoking and DLCO in idiopathic pulmonary fibrosis patients

Novel therapeutic strategies and drugs for idiopathic pulmonary fibrosis

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