Updates on the Mechanisms and Therapies of Cardiometabolic Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1065

Special Issue Editor


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Guest Editor
1. Integrated Pharma Solutions LLC, Boston, MA 02101-02117, USA
2. College of Professional Studies, Northeastern University, Boston, MA 02101-02117, USA
Interests: cell and gene therapy; cardiovascular disease; metabolic disease; atherosclerosis; dyslipidemia; animal models; drug discovery and development

Special Issue Information

Dear Colleagues,

Cardio-metabolic disorders that include cardiovascular and metabolic diseases such as diabetes are the leading cause of mortality globally. Almost 70% of patients with diabetes develop atherosclerotic cardiovascular disease (ASCVD). Metabolic pathway derangements lead to dyslipidemia and hyperglycemia and increase the risk of ASCVD by increasing glucose, oxidative stress and proatherogenic lipoproteins. Despite significant progress in targeting lipid and glucose metabolic pathways to develop new therapies for CVD treatment, reducing CVD risk in patients is still challenging. Therefore, examining novel pathways and using advanced technologies offer opportunities to understand cellular mechanisms and help develop CVD therapy.

This Special Issue focuses on the mechanism of metabolic pathways and in vitro/in vivo cellular functions to drive therapeutic approaches. New and novel cell and animal models and the use of antisense, mAbs, gene therapy and gene editing technologies now show potential to target novel pathways and tissues for CVD therapy.

Dr. Rai Ajit K. Srivastava
Guest Editor

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Keywords

  • cardiovascular disease
  • atherosclerosis
  • metabolic disease
  • hyperlipidemia
  • diabetes
  • proatherogenic lipoproteins
  • drug discovery
  • gene therapy/gene editing
  • ASO
  • mAb

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Published Papers (1 paper)

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Research

17 pages, 8251 KiB  
Article
Cell-Specific Effects of Insulin in a Murine Model of Restenosis Under Insulin-Sensitive and Insulin-Resistant Conditions
by Marel Gonzalez Medina, Zhiwei Liu, Johny Wang, Cindy Zhang, Sarah B. Cash, Carolyn L. Cummins and Adria Giacca
Cells 2024, 13(16), 1387; https://doi.org/10.3390/cells13161387 - 20 Aug 2024
Viewed by 780
Abstract
Restenosis following percutaneous revascularization is a major challenge in patients with insulin resistance and diabetes. Currently, the vascular effects of insulin are not fully understood. In vitro, insulin’s effects on endothelial cells (ECs) are beneficial, whereas on vascular smooth muscle cells (SMCs), they [...] Read more.
Restenosis following percutaneous revascularization is a major challenge in patients with insulin resistance and diabetes. Currently, the vascular effects of insulin are not fully understood. In vitro, insulin’s effects on endothelial cells (ECs) are beneficial, whereas on vascular smooth muscle cells (SMCs), they are mitogenic. We previously demonstrated a suppressive effect of insulin on neointimal growth under insulin-sensitive conditions that was abolished in insulin-resistant conditions. Here, we aimed to determine the cell-specific effects of insulin on neointimal growth in a model of restenosis under insulin-sensitive and insulin-resistant conditions. Vascular cell-specific insulin receptor (IR)-deficient mice were fed a low-fat diet (LFD) or a high-fat, high-sucrose diet (HFSD) and implanted with an insulin pellet or vehicle prior to femoral artery wire injury. In insulin-sensitive conditions, insulin decreased neointimal growth only in controls. However, under insulin-resistant conditions, insulin had no effect in either control, EC-specific or SMC-specific IR-deficient mice. These data demonstrate that EC and SMC IRs are required for the anti-restenotic effect of insulin in insulin-sensitive conditions and that, in insulin resistance, insulin has no adverse effect on vascular SMCs in vivo. Full article
(This article belongs to the Special Issue Updates on the Mechanisms and Therapies of Cardiometabolic Disease)
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