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The magnitude of the apoptosis is called arterial denudation, which elicits critical pro-atherosclerotic mechanisms, including smooth muscle cell proliferation, migration, and ECM secretion in diabetic conditions

These findings support the development of GSNO as a potential adjunct pharmacological agent or incorporated into NO releasing biomaterials to mitigate I/R injury

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In response, interconnected stressresponse pathways, including the cytosolic HSR, the UPR, and the UPRmt, act collectively to restore proteostasis

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Acknowledgements This work was supported in part by the 2023 AACR-AstraZeneca Breast Cancer Research Fellowship (J.H.), The Ludwig Cancer at Harvard Medical School (T.M.), and the NIH grants R35CA253027 (W.W.)