Molecular Pathways in Idiopathic Pulmonary Fibrosis: A Review of Novel Insights for Drug Design DOI
Dilay Kahvecioglu

Drug Development Research, Год журнала: 2025, Номер 86(3)

Опубликована: Апрель 28, 2025

ABSTRACT Idiopathic pulmonary fibrosis is a progressive, irreversible lung disease of unknown cause, characterized by gradual thickening and scarring tissue, impairing oxygen transfer into the bloodstream. As result, symptoms such as shortness breath, fatigue, persistent dry cough occur. Currently, FDA‐approved antifibrotic agents Pirfenidone Nintedanib can slow progression disease. However, these treatments cannot completely stop loss function do not provide significant improvement in quality life patients. progresses, capacity decreases, breath increases, general health deteriorates significantly. Therefore, new more effective, targeted therapies that halt IPF are urgently needed. This review addresses novel strategies to or disease‐related targeting key mechanisms involved pathogenesis IPF. The molecular structure–activity relationships (SARs) synthesized compounds JAK/STAT, TGF‐β/Smad, Wnt/β‐catenin, PI3K, JNK1, other critical signaling pathways were examined. These approaches have great potential for development potent selective therapeutic treatment insights provided this may contribute future efficient drugs.

Язык: Английский

Update of Aging Hallmarks in Idiopathic Pulmonary Fibrosis DOI Creative Commons
Ana Lilia Torres-Machorro,

Ángeles García-Vicente,

Marco Espina-Ordoñez

и другие.

Cells, Год журнала: 2025, Номер 14(3), С. 222 - 222

Опубликована: Фев. 5, 2025

Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation fibroblast populations that synthesize large amounts extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights key findings about IPF characteristics recently recognized as aging, including mechanical alterations, inflammaging, dysbiosis, alternative splicing, and disabled macroautophagy. It also revisits classic which encompass stem cell exhaustion, cellular senescence, altered intercellular communication. Enhancing our understanding fundamental processes underlie in may facilitate development innovative experimental strategies to improve therapeutic outcomes.

Язык: Английский

Процитировано

0
Integrated bioinformatics analysis screened the key genes and pathways of idiopathic pulmonary fibrosis DOI Creative Commons

Juan Wu,

Yangyang Wei,

Kang Hong

и другие.

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

Опубликована: Апрель 25, 2025

Язык: Английский

Процитировано

0
Molecular Pathways in Idiopathic Pulmonary Fibrosis: A Review of Novel Insights for Drug Design DOI
Dilay Kahvecioglu

Drug Development Research, Год журнала: 2025, Номер 86(3)

Опубликована: Апрель 28, 2025

ABSTRACT Idiopathic pulmonary fibrosis is a progressive, irreversible lung disease of unknown cause, characterized by gradual thickening and scarring tissue, impairing oxygen transfer into the bloodstream. As result, symptoms such as shortness breath, fatigue, persistent dry cough occur. Currently, FDA‐approved antifibrotic agents Pirfenidone Nintedanib can slow progression disease. However, these treatments cannot completely stop loss function do not provide significant improvement in quality life patients. progresses, capacity decreases, breath increases, general health deteriorates significantly. Therefore, new more effective, targeted therapies that halt IPF are urgently needed. This review addresses novel strategies to or disease‐related targeting key mechanisms involved pathogenesis IPF. The molecular structure–activity relationships (SARs) synthesized compounds JAK/STAT, TGF‐β/Smad, Wnt/β‐catenin, PI3K, JNK1, other critical signaling pathways were examined. These approaches have great potential for development potent selective therapeutic treatment insights provided this may contribute future efficient drugs.

Язык: Английский

Процитировано

0