Senescent AECⅡ and the implication for idiopathic pulmonary fibrosis treatment
- PMID: 36457712
- PMCID: PMC9705785
- DOI: 10.3389/fphar.2022.1059434
Senescent AECⅡ and the implication for idiopathic pulmonary fibrosis treatment
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and lethal lung disease with limited treatment options. The onset of IPF increases with age, indicating that aging is a major risk factor for IPF. Among the hallmarks of aging, cellular senescence is the primordial driver and primary etiological factor for tissue and organ aging, and an independent risk factor for the progression of IPF. In this review, we focus on the senescence of alveolar type II epithelial cells (AECIIs) and systematically summarize abnormal changes in signal pathways and biological process and implications of senescent AECIIs during IPF progression. Meanwhile, we objectively analyze current medications targeting the elimination of senescent cells or restoration of vitality such as senolytics, senomorphics, autophagy regulators, and stem cell therapy. Finally, we dialectically discuss the feasibility and limitation of targeting senescent AECIIs for IPF treatment. We hope that the understanding will provide new insights to the development of senescent AECII-based approaches for the prevention and mitigation of IPF.
Keywords: alveolar type II epithelial cells (AECIIs); cell senescence; idiopathic pulmonary fibrosis; senescence-associated secretory phenotype; senescenceassociated differentiation disorder.
Copyright © 2022 Zhang, Zhang, Lv, Li and Song.
Conflict of interest statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Figures
Similar articles
-
Cellular senescence and autophagy in the pathogenesis of chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF).Respir Investig. 2016 Nov;54(6):397-406. doi: 10.1016/j.resinv.2016.03.010. Epub 2016 May 24. Respir Investig. 2016. PMID: 27886850 Review.
-
Fibroblast Senescence in Idiopathic Pulmonary Fibrosis.Front Cell Dev Biol. 2020 Nov 25;8:593283. doi: 10.3389/fcell.2020.593283. eCollection 2020. Front Cell Dev Biol. 2020. PMID: 33324646 Free PMC article. Review.
-
Senotherapeutics: Targeting senescence in idiopathic pulmonary fibrosis.Semin Cell Dev Biol. 2020 May;101:104-110. doi: 10.1016/j.semcdb.2019.12.008. Epub 2019 Dec 24. Semin Cell Dev Biol. 2020. PMID: 31879264 Free PMC article. Review.
-
Molecular mechanisms of alveolar epithelial cell senescence and idiopathic pulmonary fibrosis: a narrative review.J Thorac Dis. 2023 Jan 31;15(1):186-203. doi: 10.21037/jtd-22-886. Epub 2022 Dec 27. J Thorac Dis. 2023. PMID: 36794134 Free PMC article. Review.
-
Curcumin analogue EF24 prevents alveolar epithelial cell senescence to ameliorate idiopathic pulmonary fibrosis via activation of PTEN.Phytomedicine. 2024 Oct;133:155882. doi: 10.1016/j.phymed.2024.155882. Epub 2024 Jul 27. Phytomedicine. 2024. PMID: 39096545
Cited by
-
Mesenchymal stem cells and pulmonary fibrosis: a bibliometric and visualization analysis of literature published between 2002 and 2021.Front Pharmacol. 2023 Jul 4;14:1136761. doi: 10.3389/fphar.2023.1136761. eCollection 2023. Front Pharmacol. 2023. PMID: 37469875 Free PMC article.
-
hucMSCs treatment prevents pulmonary fibrosis by reducing circANKRD42-YAP1-mediated mechanical stiffness.Aging (Albany NY). 2023 Jun 16;15(12):5514-5534. doi: 10.18632/aging.204805. Epub 2023 Jun 16. Aging (Albany NY). 2023. PMID: 37335082 Free PMC article.
-
The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chin Med. 2025 Feb 5;20(1):19. doi: 10.1186/s13020-025-01067-4. Chin Med. 2025. PMID: 39910395 Free PMC article. Review.
-
YAP/TAZ activation mediates PQ-induced lung fibrosis by sustaining senescent pulmonary epithelial cells.Respir Res. 2024 May 18;25(1):212. doi: 10.1186/s12931-024-02832-z. Respir Res. 2024. PMID: 38762455 Free PMC article.
-
Dysregulated bidirectional epithelial-mesenchymal crosstalk: a core determinant of lung fibrosis progression.Chin Med J Pulm Crit Care Med. 2024 Mar;2(1):27-33. doi: 10.1016/j.pccm.2024.02.001. Chin Med J Pulm Crit Care Med. 2024. PMID: 38558961 Free PMC article.
References
Publication types
LinkOut - more resources
Full Text Sources