Pamrevlumab for Idiopathic Pulmonary Fibrosis

JAMA, Год журнала: 2024, Номер 332(5), С. 380 - 380

Опубликована: Май 19, 2024

Current treatments for idiopathic pulmonary fibrosis slow the rate of lung function decline, but may be associated with adverse events that affect medication adherence. In phase 2 trials, pamrevlumab (a fully human monoclonal antibody binds to and inhibits connective tissue growth factor activity) attenuated progression without substantial events.

Язык: Английский

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Pirfenidone and Nintedanib in Pulmonary Fibrosis: Lights and Shadows

Pharmaceuticals, Год журнала: 2024, Номер 17(6), С. 709 - 709

Опубликована: Май 30, 2024

Pirfenidone and Nintedanib are specific drugs used against idiopathic pulmonary fibrosis (IPF) that showed efficacy in non-IPF fibrosing interstitial lung diseases (ILD). Both have side effects affect patients different ways levels of severity, making treatment even more challenging for clinicians. The present review aims to assess the effectiveness potential complications regimens across various ILD diseases. A detailed search was performed relevant articles published between 2018 2023 listed PubMed, UpToDate, Google Scholar, ResearchGate, supplemented with manual research. following keywords were searched databases all possible combinations: Nintedanib; Pirfenidone, disease, fibrosis. most widely accepted method evaluating progression is through decline forced vital capacity (FVC), as determined by respiratory function tests. Specifically, a decrease FVC over 6–12-month period correlates directly increased mortality rates. Antifibrotic been extensively validated; however, some reported several effects, predominantly gastrointestinal symptoms (such diarrhea, dyspepsia, vomiting), well photosensitivity skin rashes, particularly associated Pirfenidone. In cases where extremely severe threatening than disease itself, has be discontinued. However, further research needed optimize use antifibrotic agents PF-ILDs, which could slow all-cause mortality. Finally, other studies requested establish treatments can stop progression.

Язык: Английский

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Anoikis and SPP1 in idiopathic pulmonary fibrosis: integrating bioinformatics, cell, and animal studies to explore prognostic biomarkers and PI3K/AKT signaling regulation

Expert Review of Clinical Immunology, Год журнала: 2024, Номер 20(6), С. 679 - 693

Опубликована: Фев. 6, 2024

This study aims to explore the relevance of anoikis in idiopathic pulmonary fibrosis (IPF) and identify associated biomarkers signaling pathways.

Язык: Английский

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Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions

Cell Biochemistry and Biophysics, Год журнала: 2025, Номер unknown

Опубликована: Фев. 19, 2025

Abstract Idiopathic Pulmonary Fibrosis (IPF) is a severe, rapidly advancing disease that drastically diminishes life expectancy. Without treatment, it can progress to lung cancer. The precise etiology of IPF remains unknown, but inflammation and damage the alveolar epithelium are widely thought be pivotal in its development. Research has indicated activating NLRP3 inflammasome crucial mechanism pathogenesis, as triggers release pro-inflammatory cytokines such IL-1β, IL-18, TGF-β. These contribute myofibroblast differentiation extracellular matrix (ECM) accumulation. Currently, treatment options for limited. Only two FDA-approved medications, pirfenidone nintedanib, available. While these drugs decelerate progression, they come with range side effects do not cure disease. Additional strategies primarily involve supportive care therapy. Emerging research highlighted numerous flavonoids derived from traditional medicines inhibit critical regulators responsible inflammasome. show promise potential therapeutic agents managing IPF, offering new avenue targets core inflammatory processes this debilitating condition. Graphical

Язык: Английский

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Advancements in Nanotechnology for Targeted Drug Delivery in Idiopathic Pulmonary Fibrosis: A Focus on Solid Lipid Nanoparticles and Nanostructured Lipid Carriers

Drug Development and Industrial Pharmacy, Год журнала: 2025, Номер unknown, С. 1 - 18

Опубликована: Фев. 18, 2025

Objective This review aims to explore innovative therapeutic strategies, with a particular focus on recent advancements in drug delivery systems using bioinspired nanomaterials such as solid lipid nanoparticles (SLNs) and nanostructured carriers (NLCs) for the Idiopathic pulmonary fibrosis (IPF).

Язык: Английский

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Mechanisms of radiation‐induced tissue damage and response

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

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An FGF2-Derived Short Peptide Attenuates Bleomycin-Induced Pulmonary Fibrosis by Inhibiting Collagen Deposition and Epithelial–Mesenchymal Transition via the FGFR/MAPK Signaling Pathway

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(2), С. 517 - 517

Опубликована: Янв. 9, 2025

Following the COVID-19 pandemic, prevalence of pulmonary fibrosis has increased significantly, placing patients at higher risk and presenting new therapeutic challenges. Current anti-fibrotic drugs, such as Nintedanib, can slow decline in lung function, but their severe side effects highlight urgent need for safer more targeted alternatives. This study explores potential underlying mechanisms an endogenous peptide (P5) derived from fibroblast growth factor 2 (FGF2), developed by our research team. Using a bleomycin-induced mouse model, we observed that P5 alleviated inhibiting collagen deposition, confirmed CT scans histological staining. In TGF-β-induced cell models, effectively suppressed deposition epithelial–mesenchymal transition (EMT). Transcriptome analysis highlighted pathways related to receptor binding, extracellular matrix organization, adhesion, with KEGG confirming FGFR/MAPK signaling inhibition primary mechanism its effects. summary, demonstrates significantly attenuates through EMT, signaling, providing promising approach fibrosis.

Язык: Английский

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Modification of the course of disease progression in idiopathic pulmonary fibrosis by pirfenidone: evidence of the potential for disease reversal

BMJ Case Reports, Год журнала: 2025, Номер 18(3), С. e263966 - e263966

Опубликована: Март 1, 2025

Idiopathic pulmonary fibrosis (IPF) is a fibrosing pneumonia of unknown causation with chronic, progressive course that may be modified by treatment the antifibrotic agents, pirfenidone and nintedanib. Both drugs have been shown to slow disease progression, but, in rare cases, has stabilise even improve lung function. We present case patient whose function pathognomonic features on CT imaging improved significantly commencement pirfenidone. Withholding was associated functional morphological deterioration subsequently reversed stabilised following recommencement this treatment. discuss potential mechanisms might explain response, compare our others described previously consequences restricted prescribing within specified range vital capacity opportunity influence natural history IPF early before irreversible develops.

Язык: Английский

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Exercise and tissue fibrosis: recent advances in therapeutic potential and molecular mechanisms

Frontiers in Endocrinology, Год журнала: 2025, Номер 16

Опубликована: Март 20, 2025

Tissue fibrosis represents an aberrant repair process, occurring because of prolonged injury, sustained inflammatory response, or metabolic disorders. It is characterized by excessive accumulation extracellular matrix (ECM), resulting in tissue hardening, structural remodeling, and loss function. This pathological phenomenon a common feature the end stage numerous chronic diseases. Despite advent novel therapeutic modalities, including antifibrotic agents, these have only modest efficacy reversing established are associated with adverse effects. In recent years, growing body research has demonstrated that exercise significant benefits potential treatment fibrosis. The anti-fibrotic effects mediated multiple mechanisms, direct inhibition fibroblast activation, reduction expression pro-fibrotic factors such as transforming growth factor-β (TGF-β) slowing collagen deposition. Furthermore, been to assist maintaining dynamic equilibrium repair, thereby indirectly reducing damage can also help maintain balance improving disorders, exerting anti-inflammatory antioxidant effects, regulating cellular autophagy, restoring mitochondrial function, activating stem cell activity, apoptosis, alleviating tissue. paper presents review its underlying mechanisms for range fibrosis, cardiac, pulmonary, renal, hepatic, skeletal muscle. offers valuable reference point non-pharmacological intervention strategies comprehensive fibrotic

Язык: Английский

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Structure Optimization of c-Jun N-terminal Kinase 1 Inhibitors for Treating Idiopathic Pulmonary Fibrosis

Journal of Medicinal Chemistry, Год журнала: 2024, Номер unknown

Опубликована: Сен. 20, 2024

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease with an elusive etiology. Aberrant activation of c-Jun N-terminal kinase 1 (JNK1) has been implicated in its pathogenesis. Through combination structure-based drug design structure-activity relationship (SAR) optimization, series pyrimidine-2,4-diamine scaffold derivatives have developed as potent JNK1 inhibitors. Compound

Язык: Английский

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