ArticleJournal of molecular and cellular cardiology plus2025
Deletion of CHOP in beta cell protects mice from cardiovascular complications in type 2 diabetes: evidence from a pre-clinical mouse model.
Article in Journal of molecular and cellular cardiology plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Cardiovascular complications are the leading cause of morbidity and mortality in patients with type 2 diabetes (T2D), which is recognized as a major independent risk factor for coronary artery disease, stroke, peripheral vascular disease, and heart failure. The interrelationship between metabolic dysfunction and cardiovascular disease is complex and multifactorial, involving hyperglycemia, insulin resistance, inflammation, and oxidative stress. Evidence indicates that endoplasmic reticulum (ER) stress and induction of the unfolded protein response (UPR) contribute to metabolic dysregulation and vascular dysfunction. However, the specific role of beta cell-derived UPR mediators, particularly C/EBP homologous protein (CHOP), in coordinating this interorgan axis between the endocrine pancreas and the cardiovascular system remains poorly understood. Methods: To determine the role of beta cell CHOP in mediating the link between T2D and cardiovascular complications, we specifically deleted CHOP in beta cells. Thus, male and female β-cell Results: β-cell Conclusion: This study elucidates CHOP in pancreatic beta cells as a key mechanism linking T2D to cardiovascular complications. Deleting CHOP in beta cells reduces metabolic and cardiovascular issues, underscoring the role of beta cell stress in the connection between T2D and cardiovascular disease. These findings suggest that CHOP may be a potential target for preventing T2D-related cardiovascular complications.
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