Bufalin Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Macrophage Pyroptosis via P62 Pathway
Open accessAbstract
Bufalin, which is isolated from toad venom, exerts positive effects on hearts under pathological circumstance. We aimed to investigate the effects and mechanisms of bufalin on myocardial I/R injury. In vivo, bufalin ameliorated myocardial I/R injury, which characteristics with better ejection function, decreased infarct size and less apoptosis. The levels of pyroptotic proteins were increased in I/R-treated macrophages and inflammatory cytokines expressed more in I/R-induced mouse, which could be attenuated by bufalin. Bufalin also reduced H/R-treated macrophage pyroptosis in vitro. Autophagic flux blockage and ROS accumulation were reduced by bufalin in impaired macrophages. Overexpression of p62 abrogated the anti-proptosis and anti-oxidative effects of bufalin. The levels of apoptosis related proteins were changed and TUNEL-positive ratio was raised in cardiomyocytes that received conditioned medium treatment with H/R-treated macrophages, while bufalin pretreatment could reduce apoptosis. These findings indicate that bufalin may attenuate myocardial I/R injury by suppressing macrophage pyroptosis via P62 pathway.
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Bufalin induced apoptosis, necroptosis, ferroptosis, autophagy, and senescence through AMPK, RIP1/ROS, DECR1, p62, and p53 pathways.
“Bufalin induced apoptosis, necroptosis, ferroptosis, autophagy, and senescence through AMPK, RIP1/ROS, DECR1, p62, and p53 pathways5,44–48.”
From Harnessing artificial intelligence to identify Bufalin as a molecular glue degrader of estrogen receptor alpha (2025) · cites this paper as [45]
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Self-citation
- Authors
- Li, C., Ma, Z., Wei, X., Wang, Y., Wu, J., Li, X., Sun, X., Ding, Z., Yang, C., & Zou, Y.
- Affiliations
- Shanghai Medical College of Fudan University (CN)
- Fudan University (CN)
- Corresponding author
- Ding, Zhiwen
- Yang, Cheng
- Zou, Yunzeng
- Venue
- Journal of Cardiovascular Translational Research
- Published
- 2024-12-28
- Volume
- 18
- Issue
- 2
- Pages
- 221-236
- ISSN
- 1937-5387 (ISSN-L)
- 1937-5395
- PMC
- PMC12043737
- OpenAlex
- W4405861773
- Cited by
- 13
- References
- 72
- Citations by year
- 2026: 7 · 2025: 6
- FWCI
- 3.95
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Cardiovascular Translational Research (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (82230009, 82430016, 81900245)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- bufalin, myocardial ischemia-reperfusion injury, macrophage pyroptosis, autophagy, reactive oxygen species, cardiomyocyte apoptosis, inflammatory cytokines, toad venom, cardioprotection
- MeSH terms
- RAW 264.7 Cells, Pyroptosis, Sequestosome-1 Protein, Animals, Anti-Inflammatory Agents, Bufanolides, Disease Models, Animal, Macrophages, Male, Mice, Inbred C57BL, Myocardial Infarction, Signal Transduction, Myocardial Reperfusion Injury, Cytokines, Inflammation Mediators, Myocytes, Cardiac, Mice
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Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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