Pneumoconiosis is currently one of the most common occupational diseases in clinical practice. Its pathogenesis has not yet been fully elucidated, and effective clinical treatments are lacking. MicroRNAs (miRNAs) are a class of non-coding single-stranded RNA molecules that regulate gene expression at the post-transcriptional level by binding to target genes, thereby inhibiting mRNA translation or promoting mRNA degradation. Existing studies have shown that miRNAs are closely associated with the development and progression of pneumoconiosis, making them important candidate biomarkers for early screening and diagnosis of the disease. This review summarizes the current research status and advances regarding miRNAs in pneumoconiosis, aiming to provide new insights and approaches for understanding its pathogenesis, as well as for early warning, diagnosis, and treatment.

Pulmonary hypertension (PH) is a chronic and complex condition characterized by structural alterations in the pulmonary vasculature, leading to vascular remodeling, increased pulmonary vascular resistance, and heightened vasoreactivity. Although nicotine exposure is demonstrated to adversely affect the structure and function of pulmonary arteries, the underlying molecular mechanisms remain incompletely elucidated. After eight weeks of nicotine exposure, right ventricular systolic pressure (RVSP) increased in a concentration-dependent manner with nicotine doses, accompanied by a progressive reduction in tricuspid annular plane systolic excursion (TAPSE). Nicotine-treated mice exhibited a significant increase in respiratory frequency, whereas expiratory flow at 50%, peak inspiratory flow, peak expiratory flow, and tidal volume showed concentration-dependent decreases. Furthermore, pulmonary arteries from nicotine-exposed mice displayed enhanced concentration-dependent contractions in response to vasoconstrictor. Notably, partial smooth-muscle Cx43 deficiency not only depressed the changes of RVSP, TAPSE and the pulmonary function parameters but also reduced pulmonary artery hyperreactivity. Additionally, nicotine treatment significantly inhibited the contractile response of pulmonary arteries to (4-AP), which was associated with decreased protein levels of Kv1.2 and Kv2.1. Importantly, partial smooth-muscle Cx43 deficiency reversed the nicotine-induced changes in pulmonary arterial hyperreactivity, Kv1.2 and Kv2.1 expression. Collectively, Cx43 upregulation, with subsequent downregulation of Kv1.2 and Kv2.1, drives nicotine-induced pulmonary arterial dysfunction.

Silicosis is the most common occupational lung disease and association with Mycobacterium tuberculosis infection is common. Although extrapulmonary tuberculosis cases are rare, skeletal tuberculosis is responsible for 10-35% of these cases. Pott's disease is the most common form of skeletal tuberculosis, but it is not commonly encountered today. A 49-year-old male patient presented to our clinic with complaints of back pain, leg pain, and weight loss for 9 months. His occupational history revealed that he worked as a dental technician and a sandblasting for 30 years. In 2002, he was diagnosed with pneumoconiosis. Thoracovertebral Computed Tomography and Magnetic Resonance Imaging showed lytic lesions in the anterior middle columns of the T6-T9 vertebrae and an anterior narrow angle kyphosis (Gibbus deformity) at the level of T9 vertebra. The findings were primarily evaluated in favor of Pott's disease abscess. Posterior segmental instrumentation and osteotomy were performed. The patient was evaluated as extrapulmonary tuberculosis, and anti-tuberculosis treatment was started. We present a case of pneumoconiosis with extrapulmonary tuberculosis and Pott's disease.

Pneumoconiosis, characterized by progressive pulmonary fibrosis, remains a predominant occupational disease in China, with coal workers' pneumoconiosis (CWP) and silicosis being the primary subtypes. Despite extensive research, its underlying pathogenic mechanisms are not yet fully understood. Mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) are crucial subcellular microdomains that govern Ca[2+] transport, sustain cellular bioenergetics, and maintain systemic homeostasis. Emerging evidence has linked the structural and functional dysregulation of MAMs to the pathogenesis of various fibrotic disorders. Apoptosis, a highly regulated cell death process, is a key driver in pneumoconiosis progression, in which Ca[2+] imbalance serves as a critical signaling cascade. Mitofusin 2 (MFN2), a core regulator of MAMs' structural integrity, mediates mitochondrial fusion and directly bridges the ER with the outer mitochondrial membrane, thereby stabilizing ER-mitochondrial coupling. However, whether MFN2 mitigates fibrosis by preserving MAMs' integrity and subsequently suppressing Ca[2+]-dependent apoptosis remains elusive. In this study, we established SD rat and A549 cell models of CWP. Our results demonstrated that MFN2 expression was downregulated after coal dust exposure, accompanied by MAMs impairment, Ca[2+] imbalance, and increased apoptosis, which ultimately drove the pathological progression of pulmonary fibrosis. Notably, MFN2 overexpression restored MAMs' structure and Ca[2+] homeostasis, alleviated abnormal apoptosis, and subsequently inhibited fibrosis. This study highlights the importance of the MFN2-MAMs-Ca[2+]-apoptosis axis and identifies MFN2 as a potential therapeutic target for pneumoconiosis.

Objective: To establish a portable Fourier transform infrared spectroscopy (FTIR) method for determining hydrogen chloride in workplace air. Methods: In May 2025, the concentration of hydrogen chloride in the air was determined using a FTIR spectrometer within the characteristic infrared absorption wave number range of hydrogen chloride (2640 cm(-1) to 2840 cm(-1)). The technical parameters of the method were evaluated, and the results were compared with those obtained by ion chromatography. Results: The quantitative analysis model of FTIR had a concentration range of 3.03-12.13 mg/m(3), with a detection limit of 0.58 mg/m(3) and a quantification limit of 2.32 mg/m(3). The accuracy was 100.0% to 104.6%, while the intra-batch precision was 0.5% to 1.9% and the inter-batch precision was 0.4% to 2.0%. The results of the FTIR method and the ion chromatography method for the determination of hydrogen chloride showed no statistically significant difference (P>0.05). Using the measurement results at 20 ℃ as reference, the decline rates at 4 ℃ and 37 ℃ were-0.1% and 1.2%, respectively. Under relative humidity conditions of 50%, 40%, 30%, and 17%, the decline rates measured by the portable FTIR were 23.2%, 9.9%, 1.0%, and-4.6%, respectively. Conclusion: The FTIR method is suitable for rapid determination of hydrogen chloride gas concentrations in workplace air.

Objective: To explore the mechanism by which targeted deletion of Smad ubiquitin regulatory factor 2 (SMURF2/Smurf2) in alveolar type Ⅱ epithelial cells (AT2) inhibits epithelial-mesenchymal transition (EMT) in silicosis. Methods: In March 2024, in vitro experiments were conducted using a mouse AT2 cell line (MLE-12), induced by silicon dioxide (SiO(2)), and small interfering RNA (siRNA) was employed for Smurf2 gene silencing. The cells were divided into control group, SiO(2) group (250 μg/ml), empty vector plasmid (siRNA-NC) +SiO(2) group (first transfected with siRNA-NC for 24 hours and then induced with SiO(2) for 24 hours), and si-Smurf2+SiO(2) group (first transfected with si-Smurf2 for 24 hours and then induced with SiO(2) for 24 hours). In vivo experiments, 20 SPF-grade C57BL/6J mice with targeted AT2 cell Smurf2 gene knockout (Smurf2(-/-)) at 8 weeks of age were randomly divided into Smurf2(-/-) control group and Smurf2(-/-) silicosis group, with 10 mice in each group; another 20 control mice were randomly divided into Smurf2(+/+) control group and Smurf2(+/+) silicosis group, with 10 mice in each group. Mice in Smurf2(-/-) silicosis group and Smurf2(+/+) silicosis group received a single intratracheal instillation of SiO(2) suspension (5 mg per mouse, 50 μl), while the remaining groups were instilled with an equal volume of normal saline. All mice were maintained until 4 weeks post-instillation. Hematoxylin eosin (HE) staining was used to observe the pathological morphology of the lung tissue, Masson staining was used to observe the distribution and deposition of collagen, and micro-CT was used to reconstruct the three-dimensional structure of the lung. Immunofluorescence staining was used to detect the co-localization of E-cadherin (E-Ca) /alpha smooth muscle actin (α-SMA) and pro-surfactant protein C (pro-SPC) /SMURF2. Western blotting was used to quantitatively analyze the expression of SMURF2, transforming growth factor beta (TGF-β) signaling-related proteins, E-Ca, N-cadherin (N-Ca), and α-SMA. Co-immunoprecipitation was used to detect the binding effect between SMURF2 and Smad7, and in vitro ubiquitination assay was used to detect the ubiquitination of Smad7. One-way ANOVA was used for comparisons among multiple groups, and LSD test was used for pairwise comparisons when variances were homogeneous, and Tamhane's T2 test was used when variances were not homogeneous. Results: Compared with the control group, the expressions of E-Ca and Smad7 were downregulated in MLE-12 cells of the SiO(2) group, while the expressions of N-Ca, α-SMA, TGF-β1, TGF-β receptor 1 (TGF-βR1), TGF-β receptor 2 (TGF-βR2), and phosphorylated Smad2/3 (p-Smad2/3) were upregulated (P<0.05) ; SMURF2 bound to Smad7, and Smad7 bound to ubiquitin (Ub). Compared with the siRNA-NC+SiO(2) group, the expressions of E-Ca and Smad7 were upregulated in the si-Smurf2+SiO(2) group, while the expressions of N-Ca, α-SMA, TGF-β1, TGF-βR1, TGF-βR2, and p-Smad2/3 were downregulated (P<0.05), the binding of Smad7 to Ub was inhibited. Compared with the Smurf2(+/+) control group, the formation of silica nodules and collagen deposition occurred simultaneously in Smurf2(+/+) silicosis mice, and the volume of high-density shadows in the lung tissue increased, with downregulated expressions of E-Ca, Smad7, and upregulated expressions of N-Ca, α-SMA, TGF-β1, TGF-βR1, TGF-βR2, and p-Smad2/3 (P<0.05). Compared with the Smurf2(+/+) silicosis group, the area of silica nodules and collagen deposition decreased in the Smurf2(-/-) silicosis group, with upregulated expressions of E-Ca, Smad7, and downregulated expressions of N-Ca, α-SMA, TGF-β1, TGF-βR1, TGF-βR2, and p-Smad2/3 (P<0.05) . Conclusion: Targeted knockout of the Smurf2 gene in AT2 cells may inhibit EMT by regulating the TGF-β/Smad signaling pathway, thereby delaying the progression of silicosis-induced pulmonary fibrosis.

Objective: To investigate the role and mechanism of miR-129-5p in inhibiting macrophage activation and antagonizing silicosis-induced pulmonary fibrosis in mice by targeting the mitogen-activated protein kinase kinase kinase 13 (MAP3K13) /phosphorylated p38 (p-p38) signaling pathway. Methods: In July 2023, 36 C57BL/6J mice were selected and randomly divided into the control group, silicosis model group (Silicosis group), silicosis+miR-129-5p agomir negative control group (S-agoNC group), silicosis+miR-129-5p agomir group (S-ago group), silicosis+miR-129-5p antagomir negative control group (S-antaNC group), and silicosis+miR-129-5p antagomir group (S-anta group), with 6 mice in each group. Mouse alveolar macrophages (MH-S) were cultured in vitro and divided into the control group (C group) and silica (SiO(2)) -induced group (S group) ; SiO(2)+miR-129-5p agomir negative control group (S+agoNC group), SiO(2)+miR-129-5p agomir group (S+ago group), SiO(2)+miR-129-5p antagomir negative control group (S+antaNC group), and SiO(2)+miR-129-5p antagomir group (S+anta group) ; SiO(2)+MAP3K13 silencing negative control group (S+NC group), SiO(2)+MAP3K13 silencing group (S+Si group). Real-time quantitative PCR was used to detect the expression of miR-129-5p in mouse lung tissue and MH-S. Western blotting was used to detect the expression of type Ⅰ collagen (COL Ⅰ), alpha smooth muscle actin (α-SMA), monocyte chemoattractant protein-1 (MCP-1), interleukin 1β (IL-1β), inducible nitric oxide synthase (iNOS), arginase 1 (Arg-1), transforming growth factor β1 (TGF-β1), MAP3K13 and p-p38 in mouse lung tissue and MH-S. Dual luciferase reporter gene assay was used to verify the regulatory effect of miR-129-5p on the target gene MAP3K13. Immunofluorescence staining was performed to detect the co-localized expression of MAP3K13 and F4/80. HE staining and VG staining were performed to observe the pathological morphology and collagen deposition in lung tissues. micro-CT was performed to detect changes in the imaging of lung tissues in mice. Immunohistochemical staining was performed to detect the expression of MAP3K13 in lung tissues. Independent sample t-test was used for comparison between two groups, one-way ANOVA was used for multiple groups, and LSD test was used for pairwise comparison when the variances were homogeneous, and Tamhane's T2 test was used when the variances were not homogeneous. Results: Compared with the control group, the expression level of miR-129-5p in mouse lung tissue was significantly downregulated in the silicosis group (P<0.05) ; compared with the S-agoNC group, the expression level of miR-129-5p in mouse lung tissue was significantly upregulated in the S-ago group (P<0.05) ; compared with the C group, the expression level of miR-129-5p in MH-S was significantly downregulated in the S group (P<0.05). Compared with the C group, the protein expression levels of MAP3K13 and p-p38 in MH-S were significantly upregulated in the S group (P<0.05). Compared with the S+agoNC group, the protein expression levels of MCP-1, IL-1β, iNOS, Arg-1, TGF-β1, MAP3K13 and p-p38 in MH-S were significantly downregulated (P<0.05) ; compared with the S+antaNC group, the protein expression levels of the above proteins were significantly upregulated (P<0.05). Compared with the S+NC group, the expression levels of the above proteins in the S+Si group were significantly downregulated (P<0.05). Compared with the S-agoNC group, the expression levels of the above proteins in the lung tissues of mice in the S-ago group were significantly downregulated (P<0.05) ; compared with the S-antaNC group, the expression levels of the above proteins in the lung tissues of mice in the S-anta group were significantly upregulated (P<0.05). Compared with the S-agoNC group, the luciferase activity of the MAP3K13-wild-type 3' untranslated region (UTR) vector in the S-ago group was significantly decreased (P<0.01). MAP3K13 was predominantly co-localized with the macrophage marker F4/80. Compared with the C group, the expression of MAP3K13 in the S group was significantly upregulated (P<0.05) ; compared with the S+agoNC group, the expression of MAP3K13 in the S+ago group was significantly downregulated (P<0.05) ; compared with the S+antaNC group, the expression of MAP3K13 in the S+anta group was significantly upregulated (P<0.05). Compared with the control group, the formation of silicotic nodules, collagen deposition, and the proportion of high-density shadows in the lung tissues of the Silicosis group were significantly increased (P<0.05) ; compared with the S-agoNC group, the above pathological injury indicators in the S-ago group were significantly decreased (P<0.05) ; while compared with the S-antaNC group, the S-anta group was significantly increased (P<0.05). Compared with the control group, the expression of MAP3K13 in the lung tissues of the Silicosis group was significantly upregulated (P<0.05) ; compared with the S-ago NC group, the expression of MAP3K13 in the S-ago group was significantly downregulated (P<0.05) ; compared with the S-anta NC group, the expression of MAP3K13 in the S-anta group was significantly upregulated (P<0.05) . Conclusion: miR-129-5p may inhibit macrophage activation and antagonize silicosis-induced fibrosis in mice by targeting the MAP3K13/p-p38 signaling pathway.

Silicosis, one of the most common and severe forms of pneumoconiosis, remains a major occupational health concern worldwide. Given the lack of effective therapies, understanding the underlying molecular mechanisms is urgently needed. Here, we report that ALKB homolog 1 (ALKBH1), an N6-methyladenosine (m[6]A) demethylase, is upregulated in silica-induced pulmonary fibrosis and plays a pro-fibrotic role. The antifibrotic peptide Ac-SDKP inhibited Alkbh1 expression and alleviated pulmonary fibrosis. Mechanistically, ALKBH1 suppressed the biosynthesis of miR-129-5p by removing m[6]A modification from pri-miR-129-5p, thereby reducing DGCR8-mediated processing and leading to decreased mature miR-129-5p levels. Ac-SDKP reversed this process, restoring miR-129-5p expression. Functionally, overexpression of miR-129-5p attenuated silica-induced pulmonary fibrosis by suppressing macrophage activation. Collectively, these findings identify the Ac-SDKP-ALKBH1-miR-129-5p axis as a critical regulatory mechanism, with ALKBH1-mediated m[6]A demethylation of pri-miR-129-5p representing a key node and a promising therapeutic target for silicosis.

Silicosis is the most common occupational lung disease caused by respirable crystalline silica inhalation, with limited therapeutic options. Cellular senescence plays a critical role in the pathogenesis of lung diseases, while the role of senescent macrophages in silicosis remains unclear. Single-cell RNA sequencing (scRNA-seq) of healthy and silicosis human and mouse lung tissues revealed that activating transcription factor 3 (ATF3)-mediated macrophage senescence is closely linked to silicosis progression. Mechanistically, Sirtuin 6 (SIRT6)-mediated ATF3 deacetylation enhanced its nuclear transport and subsequently activated mitochondria-localized glutamic acid-rich protein (MGARP) transcription, thereby causing mitochondrial dysfunction and macrophage senescence. Senescent macrophages promoted fibroblast activation via the secreted phosphoprotein 1 (SPP1)-cluster of differentiation 44 (CD44) signaling pathway. Furthermore, the nuclear transport protein importin α and the molecular chaperone protein heat shock protein 70 (HSP70) competitively bound to ATF3, preventing its lysosomal degradation while promoting its nuclear import during macrophage senescence. Moreover, the small-molecule inhibitor Itraconazole, which targets the binding site of ATF3 and importin α, could reduce ATF3 nuclear entry, macrophage senescence, and pulmonary fibrosis (PF). Collectively, our study provided insights into the mechanism by which deacetylated ATF3 facilitates silicosis progression via increased nuclear transport and macrophage senescence, and indicated potential therapeutic targets for PF.

Benzo[a]pyrene (BaP) exposure has been associated with an increased risk of neurotoxicity, including learning and memory impairment. As an antioxidant and a potential prebiotic, geraniol is speculated the potential preventive agent against neurotoxicity. This study aims to reveal the neuroprotection of geraniol on BaP-induced neurotoxicity. The results indicate geraniol increases immunofluorescence intensity of PSD-95, and decreases the immunofluorescence intensity of Iba-1 and GFAP, as well as the level of inflammatory cytokines, and pyroptosis biomarkers. Geraniol also up-regulates the expression of tight junction proteins markedly. In addition, lipopolysaccharide (LPS), might originate from intestinal flora and closely correlated with inflammation and pyroptosis, varies in brain and serum between each group. It is summarized that the underlying mechanism of neuroprotection effect of geraniol might be located on improving intestinal physical barrier function, decreasing LPS releasing, down-regulating pyroptosis and inflammatory response, thereby alleviating neurotoxicity induced by BaP in mice model.