Hypoxia-inducible factor and cellular senescence in pulmonary aging and disease

Thapa, R; Marianesan, AB; Rekha, A; Ganesan, S; Kumari, M; Bhat, AA; Ali, H; Singh, SK; Chakraborty, A; MacLoughlin, R; Gupta, G; Dua, K

Hypoxia-inducible factor and cellular senescence in pulmonary aging and disease

Thapa, R Marianesan, AB Rekha, A Ganesan, S Kumari, M Bhat, AA Ali, H Singh, SK Chakraborty, A MacLoughlin, R Gupta, G Dua, K

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Publisher:: Springer Science and Business Media LLC
Publication Type:: Journal Article
Citation:: Biogerontology, 2025, 26, (2)
Issue Date:: 2025-04

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Field	Value	Language
dc.contributor.author	Thapa, R
dc.contributor.author	Marianesan, AB
dc.contributor.author	Rekha, A
dc.contributor.author	Ganesan, S
dc.contributor.author	Kumari, M
dc.contributor.author	Bhat, AA
dc.contributor.author	Ali, H
dc.contributor.author	Singh, SK
dc.contributor.author	Chakraborty, A
dc.contributor.author	MacLoughlin, R
dc.contributor.author	Gupta, G
dc.contributor.author	Dua, K https://orcid.org/0000-0002-7507-1159
dc.date.accessioned	2025-03-01T13:28:04Z
dc.date.available	2025-03-01T13:28:04Z
dc.date.issued	2025-04
dc.identifier.citation	Biogerontology, 2025, 26, (2)
dc.identifier.issn	1389-5729
dc.identifier.issn	1573-6768
dc.identifier.uri	http://hdl.handle.net/10453/185467
dc.description.abstract	<jats:title>Abstract</jats:title> <jats:p>Cellular senescence and hypoxia-inducible factor (HIF) signaling are crucial in pulmonary aging and age-related lung diseases such as chronic obstructive pulmonary disease idiopathic pulmonary fibrosis and lung cancer. HIF plays a pivotal role in cellular adaptation to hypoxia, regulating processes like angiogenesis, metabolism, and inflammation. Meanwhile, cellular senescence leads to irreversible cell cycle arrest, triggering the senescence-associated secretory phenotype which contributes to chronic inflammation, tissue remodeling, and fibrosis. Dysregulation of these pathways accelerates lung aging and disease progression by promoting oxidative stress, mitochondrial dysfunction, and epigenetic alterations. Recent studies indicate that HIF and senescence interact at multiple levels, where HIF can both induce and suppress senescence, depending on cellular conditions. While transient HIF activation supports tissue repair and stress resistance, chronic dysregulation exacerbates pulmonary pathologies. Furthermore, emerging evidence suggests that targeting HIF and senescence pathways could offer new therapeutic strategies to mitigate age-related lung diseases. This review explores the intricate crosstalk between these mechanisms, shedding light on how their interplay influences pulmonary aging and disease progression. Additionally, we discuss potential interventions, including senolytic therapies and HIF modulators, that could enhance lung health and longevity.</jats:p>
dc.language	en
dc.publisher	Springer Science and Business Media LLC
dc.relation.ispartof	Biogerontology
dc.relation.isbasedon	10.1007/s10522-025-10208-z
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1103 Clinical Sciences
dc.subject.classification	Gerontology
dc.subject.classification	3202 Clinical sciences
dc.title	Hypoxia-inducible factor and cellular senescence in pulmonary aging and disease
dc.type	Journal Article
utslib.citation.volume	26
utslib.for	1103 Clinical Sciences
pubs.organisational-group	University of Technology Sydney
pubs.organisational-group	University of Technology Sydney/Faculty of Health
pubs.organisational-group	University of Technology Sydney/UTS Groups
pubs.organisational-group	University of Technology Sydney/UTS Groups/Centre for Inflammation (CFI)
pubs.organisational-group	University of Technology Sydney/UTS Groups/Centre for Inflammation (CFI)/Centre for Inflammation (CFI) Associate Members
pubs.organisational-group	University of Technology Sydney/UTS Groups/Australian Research Consortium in Complementary and Integrative Medicine (ARCCIM)
pubs.organisational-group	University of Technology Sydney/UTS Groups/Stroke Research Collaborative
utslib.copyright.status	open_access	*
dc.rights.license	This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/
dc.date.updated	2025-03-01T13:28:03Z
pubs.issue	2
pubs.publication-status	Published online
pubs.volume	26
utslib.citation.issue	2

Abstract:

Abstract Cellular senescence and hypoxia-inducible factor (HIF) signaling are crucial in pulmonary aging and age-related lung diseases such as chronic obstructive pulmonary disease idiopathic pulmonary fibrosis and lung cancer. HIF plays a pivotal role in cellular adaptation to hypoxia, regulating processes like angiogenesis, metabolism, and inflammation. Meanwhile, cellular senescence leads to irreversible cell cycle arrest, triggering the senescence-associated secretory phenotype which contributes to chronic inflammation, tissue remodeling, and fibrosis. Dysregulation of these pathways accelerates lung aging and disease progression by promoting oxidative stress, mitochondrial dysfunction, and epigenetic alterations. Recent studies indicate that HIF and senescence interact at multiple levels, where HIF can both induce and suppress senescence, depending on cellular conditions. While transient HIF activation supports tissue repair and stress resistance, chronic dysregulation exacerbates pulmonary pathologies. Furthermore, emerging evidence suggests that targeting HIF and senescence pathways could offer new therapeutic strategies to mitigate age-related lung diseases. This review explores the intricate crosstalk between these mechanisms, shedding light on how their interplay influences pulmonary aging and disease progression. Additionally, we discuss potential interventions, including senolytic therapies and HIF modulators, that could enhance lung health and longevity.

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http://hdl.handle.net/10453/185467