REVIEW article
Front. Physiol.
Sec. Vascular Physiology
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1535153
This article is part of the Research TopicNew Insights on Vascular and Metabolic Diabetic ComplicationsView all 12 articles
Insulin resistance, Ca 2+ signaling alterations and vascular dysfunction in prediabetes and Metabolic Syndrome
Provisionally accepted
Tatiana Romero-García1
J. Gustavo Vazquez-Jimenez2
Rommel Sánchez-Hernández3
Jesus Alberto Olivares-Reyes4
Angélica Rueda4*- 1Facultad de Deportes, Universidad Autónoma de Baja California, Mexicali, Mexico
- 2Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali, Baja California, Mexico
- 3Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México, Mexico City, Mexico
- 4Departamento de Bioquímica, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional., Mexico City, México, Mexico
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Prediabetes and Metabolic Syndrome (MetS) share a common pathway to induce vascular dysfunction through hyperinsulinemia without the presence of overt hyperglycemia. Insulin resistance (IR) is a key factor in vascular complications in diabetes; however, vascular dysfunction has been reported in MetS patients, even in the absence of chronic hyperglycemic conditions. We consider that the alterations in the intracellular Ca2+ handling of vascular smooth muscle cells (VSMCs) and the impairment of the insulin receptor signaling pathway may contribute to the etiology of vascular diseases in prediabetes and MetS. Therefore, it is critical to understand the mechanisms by which prediabetes and MetS alter the expression and activity of proteins involved in intracellular Ca2+ signaling in VSMCs, particularly those related to vasorelaxation. The functional unit, integrated by the voltage-gated L-type Ca2+ channel (CaV1.2), the Sarco/Endoplasmic Reticulum Ca2+ ATPase (SERCA pump), the Ryanodine receptor (RyR), and the large-conductance Ca2+-activated K+ channel (BKCa), regulates the vascular tone and promotes vasorelaxation of the resistance arteries. Changes in this functional unit may contribute to vascular dysfunction. This review summarizes the most recent knowledge regarding alterations in the expression or activity of these proteins in the vasculature of experimental models with characteristics of prediabetes and MetS.
Keywords: prediabetes, metabolic syndrome, Vascular Dysfunction, insulin signaling, Calcium Signaling, SERCA pump, calcium sparks, ryanodine receptors. Non-Common abbreviations: AMPK adenosine 5'-monophosphate (AMP)-activated protein kinase
Received: 26 Nov 2024; Accepted: 12 May 2025.
Copyright: © 2025 Romero-García, Vazquez-Jimenez, Sánchez-Hernández, Olivares-Reyes and Rueda. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Angélica Rueda, Departamento de Bioquímica, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional., Mexico City, México, Mexico
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