Radiation-Induced Macrophage Senescence Impairs Resolution Programs and Drives Cardiovascular Inflammation Article Swipe
Sudeshna Sadhu
,
Christa Decker
,
Brian E. Sansbury
,
Michael Marinello
,
Allison Seyfried
,
Jennifer Howard
,
Masayuki Mori
,
Zeinab Hosseini
,
Thilaka Arunachalam
,
Aloke V. Finn
,
John M. Lamar
,
David Jourd’heuil
,
Liang Guo
,
Katherine C. MacNamara
,
Matthew Spite
,
Gabrielle Fredman
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.4049/jimmunol.2100284
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.4049/jimmunol.2100284
Radiation is associated with tissue damage and increased risk of atherosclerosis, but there are currently no treatments and a very limited mechanistic understanding of how radiation impacts tissue repair mechanisms. We uncovered that radiation significantly delayed temporal resolution programs that were associated with decreased efferocytosis in vivo. Resolvin D1 (RvD1), a known proresolving ligand, promoted swift resolution and restored efferocytosis in sublethally irradiated mice. Irradiated macrophages exhibited several features of senescence, including increased expression of p16INK4A and p21, heightened levels of SA-β-gal, COX-2, several proinflammatory cytokines/chemokines, and oxidative stress (OS) in vitro, and when transferred to mice, they exacerbated inflammation in vivo. Mechanistically, heightened OS in senescent macrophages led to impairment in their ability to carry out efficient efferocytosis, and treatment with RvD1 reduced OS and improved efferocytosis. Sublethally irradiated Ldlr−/− mice exhibited increased plaque necrosis, p16INK4A cells, and decreased lesional collagen compared with nonirradiated controls, and treatment with RvD1 significantly reduced necrosis and increased lesional collagen. Removal of p16INK4A hematopoietic cells during advanced atherosclerosis with p16-3MR mice reduced plaque necrosis and increased production of key intraplaque-resolving mediators. Our results demonstrate that sublethal radiation drives macrophage senescence and efferocytosis defects and suggest that RvD1 may be a new therapeutic strategy to limit radiation-induced tissue damage.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.4049/jimmunol.2100284
- https://www.jimmunol.org/content/jimmunol/207/7/1812.full.pdf
- OA Status
- bronze
- Cited By
- 37
- References
- 50
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3196984743
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W3196984743Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.4049/jimmunol.2100284Digital Object Identifier
- Title
-
Radiation-Induced Macrophage Senescence Impairs Resolution Programs and Drives Cardiovascular InflammationWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2021Year of publication
- Publication date
-
2021-08-30Full publication date if available
- Authors
-
Sudeshna Sadhu, Christa Decker, Brian E. Sansbury, Michael Marinello, Allison Seyfried, Jennifer Howard, Masayuki Mori, Zeinab Hosseini, Thilaka Arunachalam, Aloke V. Finn, John M. Lamar, David Jourd’heuil, Liang Guo, Katherine C. MacNamara, Matthew Spite, Gabrielle FredmanList of authors in order
- Landing page
-
https://doi.org/10.4049/jimmunol.2100284Publisher landing page
- PDF URL
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https://www.jimmunol.org/content/jimmunol/207/7/1812.full.pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
- OA URL
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https://www.jimmunol.org/content/jimmunol/207/7/1812.full.pdfDirect OA link when available
- Concepts
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Inflammation, Senescence, Macrophage, Resolution (logic), Medicine, Immunology, Neuroscience, Biology, Internal medicine, Computer science, Genetics, Artificial intelligence, In vitroTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
37Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 8, 2024: 10, 2023: 9, 2022: 9, 2021: 1Per-year citation counts (last 5 years)
- References (count)
-
50Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| publication_date | 2021-08-30 |
| publication_year | 2021 |
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