Special Issue "Advances in Endothelial Signaling and Function in Diabetes"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 31 January 2024 | Viewed by 757

Special Issue Editors

1. Division of Neonatology, Mount Sinai Medical Center, Miami Beach, FL 33140, USA
2. Department of Pediatrics, Florida International University School of Medicine, Miami, FL 33199, USA
Interests: endothelial nitric oxide; pulsatile shear stress; ischemia reperfusion; endothelium
Departments of Medicine and Biomedical Engineering, School of Engineering and School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: microfluidics; bioMEMS; tissue engineering; tissue chips; microphysiological systems
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Special Issue Information

Dear Colleagues,

Diabetes mellitus (DM) has reached epidemic proportions around the world and is a major public health problem. DM-related complications affect nearly every organ system in the body. The vascular endothelium lines all blood vessels and the heart and serves as a conduit for blood and a barrier between the intravascular space and organs and tissues in the body. The endothelium plays a critical role both in normal physiology and in the pathophysiology of various diseases. In DM, hyperglycemia directly affects the endothelium, resulting in the dysfunction of vascular endothelial cells that leads to a myriad of signaling locally and distally throughout the body. This Special Issue seeks to gather the latest information on how DM affects endothelial signaling and function at the cellular and whole organ level and how these findings can be used to identify therapeutic strategies to treat DM.

Prof. Dr. Jose Adams
Prof. Dr. Palaniappan Sethu
Guest Editors

Manuscript Submission Information

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  • diabetes
  • endothelium
  • endothelial cell
  • endothelial signaling
  • endothelial function
  • endothelial activation
  • cellular signaling
  • vascular signaling
  • nitric oxide
  • shear stress
  • insulin
  • oxidative stress
  • glucose

Published Papers (1 paper)

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17 pages, 2948 KiB  
Enhancing Muscle Intracellular Ca2+ Homeostasis and Glucose Uptake: Passive Pulsatile Shear Stress Treatment in Type 2 Diabetes
Biomedicines 2023, 11(10), 2596; https://doi.org/10.3390/biomedicines11102596 - 22 Sep 2023
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Type 2 diabetes mellitus (T2D) is a significant global public health problem that has seen a substantial increase in the number of affected individuals in recent decades. In a murine model of T2D (db/db), we found several abnormalities, including aberrant intracellular calcium concentration [...] Read more.
Type 2 diabetes mellitus (T2D) is a significant global public health problem that has seen a substantial increase in the number of affected individuals in recent decades. In a murine model of T2D (db/db), we found several abnormalities, including aberrant intracellular calcium concentration ([Ca2+]i), decreased glucose transport, increased production of reactive oxygen species (ROS), elevated levels of pro-inflammatory interleukins and creatine phosphokinase (CK), and muscle weakness. Previously, we demonstrated that passive pulsatile shear stress, generated by sinusoidal (headward–forward) motion, using a motion platform that provides periodic acceleration of the whole body in the Z plane (pGz), induces the synthesis of nitric oxide (NO) mediated by constitutive nitric oxide synthase (eNOS and nNOS). We investigated the effect of pGz on db/db a rodent model of T2D. The treatment of db/db mice with pGz resulted in several beneficial effects. It reduced [Ca2+]i overload; enhanced muscle glucose transport; and decreased ROS levels, interleukins, and CK. Furthermore, pGz treatment increased the expression of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS), and neuronal nitric oxide synthase (nNOS); reduced inducible nitric oxide synthase (iNOS); and improved muscle strength. The cytoprotective effects of pGz appear to be mediated by NO, since pretreatment with L-NAME, a nonspecific NOS inhibitor, abolished the effects of pGz on [Ca2+]i and ROS production. Our findings suggest that a non-pharmacological strategy such as pGz has therapeutic potential as an adjunct treatment to T2D. Full article
(This article belongs to the Special Issue Advances in Endothelial Signaling and Function in Diabetes)
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