PI3K/Akt in IPF: untangling fibrosis and charting therapies
Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive lung disease characterized by abnormal epithelial repair, persistent inflammation, and excessive extracellular matrix deposition, leading to irreversible scarring and respiratory failure. Central to its pathogenesis is the dysregulation o...
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Frontiers Media S.A.
2025-03-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1549277/full |
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| author | Janki Bhatt Janki Bhatt Alessandra Ghigo Alessandra Ghigo Emilio Hirsch Emilio Hirsch |
| author_facet | Janki Bhatt Janki Bhatt Alessandra Ghigo Alessandra Ghigo Emilio Hirsch Emilio Hirsch |
| author_sort | Janki Bhatt |
| collection | DOAJ |
| description | Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive lung disease characterized by abnormal epithelial repair, persistent inflammation, and excessive extracellular matrix deposition, leading to irreversible scarring and respiratory failure. Central to its pathogenesis is the dysregulation of the PI3K/Akt signaling pathway, which drives fibroblast activation, epithelial-mesenchymal transition, apoptosis resistance, and cellular senescence. Senescent cells contribute to fibrosis through the secretion of pro-inflammatory and profibrotic factors in the senescence-associated secretory phenotype (SASP). Current antifibrotic therapies, Nintedanib and Pirfenidone, only slow disease progression and are limited by side effects, highlighting the need for novel treatments. This review focuses on the role of PI3K/Akt signaling in IPF pathogenesis, its intersection with inflammation and fibrosis, and emerging therapeutic approaches targeting molecules along this pathway. |
| format | Article |
| id | doaj-art-f58eaa0db80f468cb1cd627e1d3c6713 |
| institution | DOAJ |
| issn | 1664-3224 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj-art-f58eaa0db80f468cb1cd627e1d3c67132025-08-20T03:03:12ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-03-011610.3389/fimmu.2025.15492771549277PI3K/Akt in IPF: untangling fibrosis and charting therapiesJanki Bhatt0Janki Bhatt1Alessandra Ghigo2Alessandra Ghigo3Emilio Hirsch4Emilio Hirsch5Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center “Guido Tarone”, University of Turin, Turin, ItalyKither Biotech S.r.l., Turin, ItalyDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center “Guido Tarone”, University of Turin, Turin, ItalyKither Biotech S.r.l., Turin, ItalyDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center “Guido Tarone”, University of Turin, Turin, ItalyKither Biotech S.r.l., Turin, ItalyIdiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive lung disease characterized by abnormal epithelial repair, persistent inflammation, and excessive extracellular matrix deposition, leading to irreversible scarring and respiratory failure. Central to its pathogenesis is the dysregulation of the PI3K/Akt signaling pathway, which drives fibroblast activation, epithelial-mesenchymal transition, apoptosis resistance, and cellular senescence. Senescent cells contribute to fibrosis through the secretion of pro-inflammatory and profibrotic factors in the senescence-associated secretory phenotype (SASP). Current antifibrotic therapies, Nintedanib and Pirfenidone, only slow disease progression and are limited by side effects, highlighting the need for novel treatments. This review focuses on the role of PI3K/Akt signaling in IPF pathogenesis, its intersection with inflammation and fibrosis, and emerging therapeutic approaches targeting molecules along this pathway.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1549277/fullidiopathic pulmonary fibrosisPI3K/AKTinflammationfibrosissenescencePI3K inhibitor |
| spellingShingle | Janki Bhatt Janki Bhatt Alessandra Ghigo Alessandra Ghigo Emilio Hirsch Emilio Hirsch PI3K/Akt in IPF: untangling fibrosis and charting therapies Frontiers in Immunology idiopathic pulmonary fibrosis PI3K/AKT inflammation fibrosis senescence PI3K inhibitor |
| title | PI3K/Akt in IPF: untangling fibrosis and charting therapies |
| title_full | PI3K/Akt in IPF: untangling fibrosis and charting therapies |
| title_fullStr | PI3K/Akt in IPF: untangling fibrosis and charting therapies |
| title_full_unstemmed | PI3K/Akt in IPF: untangling fibrosis and charting therapies |
| title_short | PI3K/Akt in IPF: untangling fibrosis and charting therapies |
| title_sort | pi3k akt in ipf untangling fibrosis and charting therapies |
| topic | idiopathic pulmonary fibrosis PI3K/AKT inflammation fibrosis senescence PI3K inhibitor |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1549277/full |
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