{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T05:55:32Z","timestamp":1790574932686,"version":"4.1.0"},"reference-count":187,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>The stepwise movement of oxygen from the atmosphere to the mitochondria, the \u201coxygen cascade\u201d, is one of the most tightly regulated systems in physiology. Despite decades of mechanistic study, it has remained quite unexplored in Geroscience. This oversight should be reconsidered. In young organisms, hypoxic stress (whether environmental or tissue\u2010specific) activates a complex adaptive response to preserve energetic stability via restraining anabolic pathways, optimizing mitochondrial performance, and reinforcing cellular quality control systems. With advancing age, angiostatic signaling increases, endothelial metabolism becomes dysregulated, and overall alveolar ventilation and pulmonary gas exchange (ventilation\u2013perfusion matching and diffusion capacity) become less efficient. These changes promote microvascular rarefaction and low\u2010grade but persistent mismatches between oxygen delivery and demand at the tissue level, ultimately destabilizing cellular function. In this review, we propose that the gradual erosion of oxygen homeostasis is not simply a byproduct of aging, but also a driver of molecular damage and functional decline. We examine the aging oxygen cascade through the framework of resilience biology, focusing on mechanisms such as mitochondrial electron leaks, oxidative stress amplification, iron dyshomeostasis, ferroptosis, and epigenetic remodeling. We also discuss interventions that alter oxygen availability, such as intermittent hypoxia, hyperbaric oxygen therapy, and hypoxic\u2013hyperoxic training. These approaches demonstrate adaptive potential, but they also highlight the narrow margin between beneficial stress and injury. We propose \u201cOxygenaging\u201d as a unifying framework in which aging associates with the progressive loss of equilibrium across the oxygen cascade, linking systemic oxygen transport to mitochondrial function, genomic stability, and cellular resilience.<\/jats:p>","DOI":"10.1111\/acel.70664","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T12:15:57Z","timestamp":1787919357000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Oxygenaging: A Physiological Framework for Geroscience"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0669-1618","authenticated-orcid":false,"given":"Stefano","family":"Donega","sequence":"first","affiliation":[{"name":"Translational Gerontology Branch (TGB), National Institute on Aging (NIA), Intramural Research Program (IRP) National Institutes of Health (NIH)  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth W.","family":"Fishbein","sequence":"additional","affiliation":[{"name":"Laboratory of Clinical Investigation (LCI), NIA, IRP, NIH  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Dominelli","sequence":"additional","affiliation":[{"name":"Faculty of Kinesiology University of Calgary  Calgary Alberta Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allison B.","family":"Herman","sequence":"additional","affiliation":[{"name":"Laboratory of Cardiovascular Science (LCS), NIA, IRP, NIH  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rafael","family":"de Cabo","sequence":"additional","affiliation":[{"name":"Translational Gerontology Branch (TGB), National Institute on Aging (NIA), Intramural Research Program (IRP) National Institutes of Health (NIH)  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myriam","family":"Gorospe","sequence":"additional","affiliation":[{"name":"Laboratory of Genetics and Genomics (LGG), NIA, IRP, NIH  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6273-1613","authenticated-orcid":false,"given":"Luigi","family":"Ferrucci","sequence":"additional","affiliation":[{"name":"Translational Gerontology Branch (TGB), National Institute on Aging (NIA), Intramural Research Program (IRP) National Institutes of Health (NIH)  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,28]]},"reference":[{"key":"e_1_2_17_2_1","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2019.00427"},{"key":"e_1_2_17_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12928"},{"key":"e_1_2_17_4_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0610131104"},{"key":"e_1_2_17_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/s42003-025-07896-1"},{"key":"e_1_2_17_6_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00204-023-03483-7"},{"key":"e_1_2_17_7_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0055953"},{"key":"e_1_2_17_8_1","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1973.34.2.137"},{"key":"e_1_2_17_9_1","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00964.2005"},{"key":"e_1_2_17_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2019.03.031"},{"key":"e_1_2_17_11_1","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00166.2018"},{"key":"e_1_2_17_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2016.05.011"},{"key":"e_1_2_17_13_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.aau5870"},{"key":"e_1_2_17_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.trci.2017.01.002"},{"key":"e_1_2_17_15_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12877-019-1184-1"},{"key":"e_1_2_17_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.resp.2004.12.009"},{"key":"e_1_2_17_17_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00166-09"},{"issue":"4","key":"e_1_2_17_18_1","article-title":"Hyperbaric Oxygenation for Tumour Sensitisation to Radiotherapy","volume":"4","author":"Bennett M. 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