Senescent Cardiac Fibroblast Is Critical for Cardiac Fibrosis after Myocardial Infarction
Open accessAbstract
Senescence is a recognized mechanism of cardiovascular diseases; however, its contribution to myocardial fibrosis and rupture after infarction and the underlying mechanisms remain unclear. Here we showed that senescent cardiac fibroblasts markedly accumulated in heart after myocardial infarction. The expression of key senescence regulators, especially p53, was significantly up-regulated in the infarcted heart or hypoxia-treated fibroblasts. Furthermore, knockdown of endogenous p53 by siRNA in fibroblasts markedly reduced hypoxia-induced cell senescence, cytokine expression but increased collagen expression, whereas increased expression of p53 protein by adenovirus infection had opposite effects. Consistent with in vitro results in cardiac fibroblasts, p53 deficiency in vivo significantly decreased the accumulation of senescent fibroblasts, the infiltration of macrophages and matrix metalloproteinases, but enhanced collagen deposition after myocardial infarction. In conclusion, these results suggest that the p53-mediated fibroblast senescence limits cardiac collagen production, and inhibition of p53 activity could represent a novel therapeutic target to increase reparative fibrosis and to prevent heart rupture after myocardial infarction.
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Myocardial infarction in mice is associated with increased senescence markers in cardiomyocytes and cardiac fibroblasts.
“Myocardial infarction in mice was associated with increased expression of senescence-associated markers such as CDKN2A and CDKN1A, SA-β-gal activity, TAF and increased expression of SASP components in mouse cardiomyocytes67 and cardiac fibroblasts68.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [68]
The Results section (‘Senescent fibroblasts accumulate in the infarcted heart in vivo’; page unavailable) reports increased SA-β-gal, p16 and p21 staining after infarction in mice and identifies the senescent cells as myofibroblasts. This supports the cardiac-fibroblast portion attached to this citation, but our copy does not report increased TAF; the cardiomyocyte portion is attached to a different citation. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSenescence-associated secretory phenotype factors aid wound healing by attracting immune cells that remove dead cells, supporting angiogenesis, restricting fibrosis, and promoting wound closure.
“SASP has recently been shown to have a beneficial effect on wound healing by recruiting immune cells to clear dead cells, promote angiogenesis, limit fibrosis, and stimulate wound closure (100, 111, 112).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [111]
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- Authors
- Zhu, F., Li, Y., Zhang, J., Piao, C., Liu, T., Li, H.-H., & Du, J.
- Affiliations
- Capital Medical University (CN)
- Corresponding author
- Du, Jie
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-09-11
- Volume
- 8
- Issue
- 9
- Pages
- e74535
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3770549
- OpenAlex
- W2057630805
- Cited by
- 201
- References
- 46
- Citations by year
- 2026: 6 · 2025: 21 · 2024: 12 · 2023: 22 · 2022: 20 · 2021: 23 · 2020: 22 · 2019: 13 · 2018: 20 · 2017: 18 · 2016: 12 · 2015: 9 · 2014: 2
- FWCI
- 5.21
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (31090363, 81025001, 2012CB517802, 81230006)
- Ministry of Science and Technology of the People's Republic of China (2012CB945104)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- cellular senescence, cardiac fibroblasts, myocardial infarction, myocardial fibrosis, p53, hypoxia, collagen deposition, macrophage infiltration, matrix metalloproteinases, cardiac rupture, therapeutic target
- MeSH terms
- Adenoviridae, Animals, Cell Movement, Cells, Cultured, Collagen, Disease Models, Animal, Endomyocardial Fibrosis, Fibroblasts, Gene Expression Regulation, Genetic Vectors, Male, Myocardial Infarction, Myocardium, Signal Transduction, Cell Hypoxia, Tumor Suppressor Protein p53, Cellular Senescence, Mice, Knockout, RNA, Small Interfering, Mice
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