Publications by authors named "Chen Wanpei"

We explored physiological effects of the sodium-glucose co-transporter-2 inhibitor empagliflozin on intact experimentally hypertrophic murine hearts following transverse aortic constriction (TAC). Postoperative drug (2-6 weeks) challenge resulted in reduced late Na currents, and increased phosphorylated (p-)CaMK-II and Nav1.5 but not total (t)-CaMK-II, and Na/Ca exchanger expression, confirming previous cardiomyocyte-level reports.

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Metabolism is one of the vital functions of cells and living organisms, and the systems to sense and respond to the metabolic alterations play pivotal roles in a plethora of biological processes, including cell proliferative activities, immune cell functions, aging processes, and neuronal functions. Recently, we have reported that a transcriptional cofactor, C-terminal binding protein 2 (CtBP2), serves as a critical metabolite sensor in this context. CtBP2 has a structural pocket called Rossmann fold to accommodate metabolites, and it has been reported to be activated upon binding to NADH/NAD.

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Article Synopsis
  • In the early stages of obesity, insulin secretion increases as a protective measure to keep glucose levels stable, but this can’t last forever, leading to the failure of β cells and the onset of diabetes.
  • The protein CtBP2 plays a vital role in regulating insulin gene expression in β cells by interacting with another factor, NEUROD1, which helps to open up chromatin at the insulin gene promoter.
  • Reduced levels of CtBP2 in pancreatic islets are observed in both mouse models and humans with obesity, and mice lacking CtBP2 specifically in β cells show glucose intolerance and impaired insulin secretion, indicating its importance in maintaining β cell health and offering potential targets for obesity-related treatments.
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Article Synopsis
  • Maintaining the balance of metabolism is really important, but too much food can mess it up, especially in obesity.
  • Researchers found out how two important proteins, PPARα and CtBP2, interact in a way that can slow down fat processing when there's extra fat in the body.
  • In obese people, this interaction gets stronger, making it harder for the body to break down fat, which could lead to new treatments for obesity-related diseases.
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Anti-PD-L1 therapy exhibits durable efficacy, but only in a small fraction of cancer patients. The immunosuppressive tumor microenvironment (TME) is a crucial obstacle that impedes cancer immunotherapy. Here, we found that anti-PD-L1 therapy coupled with CD4 T cell depletion induced colorectal tumor regression and vascular normalization, while monotherapy only retarded tumor growth without affecting the tumor vasculature.

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Background: Dexmedetomidine is a widely used anaesthetic adjuvant for cancer resection surgeries. However, recent reports suggest that it may promote tumour growth or metastasis, so it is essential to clarify its tumour-related effects.

Methods: Seven syngeneic murine tumour models were used to assess the impact of dexmedetomidine on primary tumour growth, spontaneous tumour metastasis, and surgical resection-associated metastasis.

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