Quantitative proteomics reveals the mechanism of endoplasmic reticulum stress-mediated pulmonary fibrosis in mice DOI Creative Commons

H. Li,

Jin Wang, Ziling Li

и другие.

Heliyon, Год журнала: 2024, Номер 10(20), С. e39150 - e39150

Опубликована: Окт. 1, 2024

Pulmonary fibrosis is a progressive disease that can lead to respiratory failure. Many types of cells are involved in the progression pulmonary fibrosis. This study utilized quantitative proteomics investigate mechanism TGF-β-induced fibrosis-like changes mouse epithelial cells. Our findings revealed TGF-β significantly impacted biological processes related endoplasmic reticulum, mitochondrion, and ribonucleoprotein complex. Pull-down assay coupled with identified 114 proteins may directly interact TGF-β, their functions were mitochondria, translation, ubiquitin ligase conjugation, mRNA processing, actin binding. Among them, 17 molecules also found different expression (DEPs) proteomic, such as H1F0, MED21, SDF2L1, DAD1, TMX1. Additionally, decreased folded structure number ribosomes reticulum increased key unfolded protein response, including HRD1, PERK, ERN1. Overall, our suggested induced fibrotic lung by ER stress initiated response through PRKCSH/IRE1 PERK/GADD34/CHOP signaling pathways.

Язык: Английский

Anti-TGF-β/PD-L1 bispecific antibody synergizes with radiotherapy to enhance antitumor immunity and mitigate radiation-induced pulmonary fibrosis DOI Creative Commons
Yuze Wu,

Yuheng Yan,

Yarong Guo

и другие.

Journal of Hematology & Oncology, Год журнала: 2025, Номер 18(1)

Опубликована: Март 5, 2025

Despite the success of immune checkpoint inhibitors (ICIs) in multiple malignant tumors, a significant proportion patients remain unresponsive to treatment. Radiotherapy (RT) elicits immunogenic antitumor responses but concurrently activates several evasion mechanisms. Our earlier research demonstrated efficacy YM101, an anti-TGF-β/PD-L1 bispecific antibody, stroma-rich tumors. Nevertheless, YM101 has reduced effectiveness non-inflamed tumors characterized by poor cell infiltration. This study investigated potential synergy between RT and overcoming immunotherapy resistance mitigating RT-induced pulmonary fibrosis. The activity survival outcomes plus treatment vivo were explored murine tumor models. Furthermore, inhibition metastases was assessed metastasis model. impact on dendritic (DC) maturation quantified flow cytometry, whereas cytokine chemokine secretions measured ELISA. To comprehensively characterize changes microenvironment, we utilized combination methods, including IHC staining, multiplex inmunofluorecence RNA sequencing. Additionally, evaluated significantly inhibited growth, prolonged compared with monotherapies promoted DC dose-dependent manner increased proinflammatory cytokines. Mechanistically, simultaneously infiltration activation intratumoral DCs tumor-infiltrating lymphocytes reshaped microenvironment landscape. Notably, attenuated both peritumoral fibrosis findings suggest that combined enhances immunity overcomes preclinical models, while showing therapy demonstrates promise ICI resistance, potentially sparing normal tissue, thereby providing strong rationale for further clinical investigations.

Язык: Английский

Процитировано

3

Mechanisms of radiation‐induced tissue damage and response DOI Creative Commons

Zhou Lin,

Jiaojiao Zhu, Yuhao Liu

и другие.

MedComm, Год журнала: 2024, Номер 5(10)

Опубликована: Сен. 20, 2024

Radiation-induced tissue injury (RITI) is the most common complication in clinical tumor radiotherapy. Due to heterogeneity response of different tissues radiation (IR), radiotherapy will cause types and degrees RITI, which greatly limits application Efforts are continuously ongoing elucidate molecular mechanism RITI develop corresponding prevention treatment drugs for RITI. Single-cell sequencing (Sc-seq) has emerged as a powerful tool uncovering mechanisms identifying potential targets by enhancing our understanding complex intercellular relationships, facilitating identification novel cell phenotypes, allowing assessment spatiotemporal developmental trajectories. Based on comprehensive review we analyzed regulatory networks combination with Sc-seq summarized targeted intervention pathways therapeutic Deciphering diverse underlying can shed light its pathogenesis unveil new avenues potentially facilitate repair or regeneration currently irreversible Furthermore, discuss how personalized strategies based offer promise mitigating

Язык: Английский

Процитировано

8

Clinical development complexity of TGF-β inhibition: From fibrosis to cancer immunotherapy DOI
Gabriel Gallo-Oller,

María Isabel Guillén-Antonini,

Javier Dotor

и другие.

International review of cell and molecular biology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Diagnosis and treatment of radiation induced pneumonitis in patients with lung cancer: An ESTRO clinical practice guideline DOI Creative Commons

Dirk De Ruysscher,

Els Wauters, Verena Jendrossek

и другие.

Radiotherapy and Oncology, Год журнала: 2025, Номер unknown, С. 110837 - 110837

Опубликована: Апрель 1, 2025

The incidence of radiation pneumonitis (RP) has decreased significantly compared to historical series, mainly due improved radiotherapy techniques and patient selection. Nevertheless, some patients still develop RP. This guideline provides user-friendly flowcharts address common clinical practice questions regarding We summarize the current state art mechanisms, risk factors, diagnosis treatment Dosimetric constraints minimize RP, as well factors for developing such idiopathic pulmonary fibrosis (IPF) were identified. combination medication a factor development RP was reviewed. remains exclusion, but an algorithm reaching been proposed. Finally, practical approaches are outlined.

Язык: Английский

Процитировано

0

ITGAV, a specific biomarker associated with the pathogenesis of idiopathic pulmonary fibrosis DOI Creative Commons
Zhangyang Bi, Xiaodong Wang, Xue Liu

и другие.

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Май 15, 2025

Objective Idiopathic pulmonary fibrosis (IPF), which radiologically/pathologically manifests mainly as usual interstitial pneumonia (UIP), is easily confused with chronic hypersensitivity pneumonitis (CHP) and collagenous vascular disease in clinical settings, affecting the physician's diagnosis treatment. Accurate identification of IPF from various diseases presenting UIP essential for effective therapy. Methods Gene expression data CHP, IPF, rheumatoid arthritis-UIP samples were downloaded GEO database, specific biomarkers identified to differentiate idiopathic UIP/IPF secondary UIP. We compared gene between control, UIP, groups. The mechanism PF was explored by immunohistochemistry, quantitative polymerase chain reaction, immunofluorescence, flow cytometry. Results integrin alpha V (ITGAV) a biomarker distinguishing observed gradual increase ITGAV across Animal studies indicated that elevated immune cells, particularly monocyte-derived macrophages, contributed development PF. Conclusion linked pathogenesis IPF. provides new perspectives diagnosis, mechanistic drug

Язык: Английский

Процитировано

0

Therapieinduzierte Pneumonitis in der Thoraxonkologie DOI

Kaija Leonie Minuth-Fuchs,

Christian Schulz

Deleted Journal, Год журнала: 2025, Номер unknown

Опубликована: Май 27, 2025

Процитировано

0

Regulation of idiopathic pulmonary fibrosis: a cross-talk between TGF-β signaling and MicroRNAs DOI Creative Commons
Shuo Wang,

Hanming Yu,

Shi Liu

и другие.

Frontiers in Medicine, Год журнала: 2024, Номер 11

Опубликована: Сен. 25, 2024

Pulmonary fibrosis (PF) is a highly complex and challenging disease affecting the respiratory system. Patients with PF usually have an abbreviated survival period consequential high mortality rate after diagnosis confirmed, posing serious threats to human health. In clinical practice, typically treated by antifibrotic agents, such as Pirfenidone Nintedanib. However, these agents been reported correlate substantial adverse effects, escalating costs, insufficient efficacy. Moreover, it remains unclarified about multifactorial pathology of PF. Therefore, there urgent demand for elucidating underlying mechanisms identifying safe, efficient, targeted therapeutic strategies treatment. The crucial role transforming growth factor- β (TGF-β) signaling pathway in development has explored many studies. MicroRNAs (miRNAs), which function post-transcriptional regulators gene expression, can significantly affect modulating TGF- signaling. turn, TGF-β regulate expression biogenesis miRNAs, thereby substantially progression Hence, that focus on drug-targeted regulation either augmenting down-regulated miRNAs or inhibiting overexpressed may hinder pathways related These contribute prevention suppression provide novel insights into treatment this disease.

Язык: Английский

Процитировано

2

High-dose vitamin C attenuates radiation-induced pulmonary fibrosis by targeting S100A8 and S100A9 DOI Creative Commons
Li Ma, Yu Jin,

Aifeina Aili

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2024, Номер 1870(7), С. 167358 - 167358

Опубликована: Июль 18, 2024

Radiation-induced pulmonary fibrosis (RIPF) is a frequently encountered late complication in patients undergoing radiation therapy, presenting substantial risk to patient mortality and quality of life. The pathogenesis RIPF remains unclear, current treatment options are limited efficacy. High-dose vitamin C has demonstrated potential when used conjunction with other adjuvant therapies due potent anticancer properties. However, the relationship between high-dose not yet been explored existing literature. In our study, model LLC tumor were as two animal models explore how can improve without hampering antitumour efficacy radiotherapy. impact on was assessed through various assays, including micro-CT, HE staining, Masson immunohistochemistry. Our results indicated that administering 2 days before continuing for duration 6 weeks significantly inhibited progression RIPF. order mechanism by which attenuates RIPF, we utilized RNA-seq analysis mouse lung tissue publicly available databases. findings inhibits differentiation fibroblasts into myofibroblasts targeting S100A8 S100A9 derived from neutrophils. Additionally, combination enhanced inhibition growth murine model. These revealed radiotherapy may offer promising therapeutic approach clinical management thoracic tumors prevention

Язык: Английский

Процитировано

1

Quantitative proteomics reveals the mechanism of endoplasmic reticulum stress-mediated pulmonary fibrosis in mice DOI Creative Commons

H. Li,

Jin Wang, Ziling Li

и другие.

Heliyon, Год журнала: 2024, Номер 10(20), С. e39150 - e39150

Опубликована: Окт. 1, 2024

Pulmonary fibrosis is a progressive disease that can lead to respiratory failure. Many types of cells are involved in the progression pulmonary fibrosis. This study utilized quantitative proteomics investigate mechanism TGF-β-induced fibrosis-like changes mouse epithelial cells. Our findings revealed TGF-β significantly impacted biological processes related endoplasmic reticulum, mitochondrion, and ribonucleoprotein complex. Pull-down assay coupled with identified 114 proteins may directly interact TGF-β, their functions were mitochondria, translation, ubiquitin ligase conjugation, mRNA processing, actin binding. Among them, 17 molecules also found different expression (DEPs) proteomic, such as H1F0, MED21, SDF2L1, DAD1, TMX1. Additionally, decreased folded structure number ribosomes reticulum increased key unfolded protein response, including HRD1, PERK, ERN1. Overall, our suggested induced fibrotic lung by ER stress initiated response through PRKCSH/IRE1 PERK/GADD34/CHOP signaling pathways.

Язык: Английский

Процитировано

0