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The prevalence of gestational diabetes mellitus (GDM) has increased in recent years, along with the higher prevalence of obesity in women of reproductive age. GDM is a pathology associated with vascular dysfunction in the fetoplacental unit. GDM-associated endothelial dysfunction alters the transfer of nutrients to the foetus affecting newborns and pregnant women. Various mechanisms for this vascular dysfunction have been proposed, of which the most studied are metabolic alterations of the vascular endothelium. However, different cell types are involved in GDM-associated endothelial dysfunction, including platelets. Platelets are small, enucleated cell fragments that actively take part in blood haemostasis and thrombus formation. Thus, they play crucial roles in pathologies coursing with endothelial dysfunction, such as atherosclerosis, cardiovascular diseases, and diabetes mellitus. Nevertheless, platelet function in GDM is understudied. Several reports show a potential relationship between platelet volume and mass with GDM; however, platelet roles and signaling mechanisms in GDM-associated endothelial dysfunction are unclear. This review summarizes the reported findings and proposes a link among altered amount, volume, mass, reactivity, and function of platelets and placenta development, resulting in fetoplacental vascular dysfunction in GDM.
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http://dx.doi.org/10.1111/apha.13940 | DOI Listing |
Korean J Physiol Pharmacol
September 2025
Department of Physiology & Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Diabetes mellitus is a major global health concern associated with micro-and macrovascular complications. Among the diverse mechanisms that contribute to vascular dysfunction in diabetes, endothelial to mesenchymal transition (EndMT) has emerged as a key pathological process. EndMT involves the loss of endothelial cell characteristics and the acquisition of mesenchymal features, resulting in impaired endothelial function, increased fibrosis, and inflammation.
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September 2025
Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN 55902, USA; Department of Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55902, USA.
Under physiological conditions, amyloid precursor protein (APP) is critically important for normal brain development, neurogenesis, neuronal survival, and synaptic signaling. Dyshomeostasis of APP increases deposition and accumulation of amyloid β (Aβ) in the brain parenchyma and cerebral blood vessels thereby leading to development of Alzheimer's disease and cerebral amyloid angiopathy. In this review, we critically examine existing literature supporting the concept that endothelial APP performs important vascular protective functions in the brain.
View Article and Find Full Text PDFJ Photochem Photobiol B
September 2025
The First Affiliated Hospital, Department of Ophthalmology, Hengyang Medical school, University of South China, Hengyang, Hunan 421001, China; Xiamen University Affiliated Xiamen Eye Center, Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Fujian Engineering and Research Center
Blue light, defined as short-wavelength visible light ranging from 400 to 500 nm, is recognized for its high energy within the visible light spectrum. The prevalent use of light-emitting diodes (LEDs) has significantly increased exposure to blue light. Corneal endothelial cells (CECs) playing a crucial role in maintaining corneal transparency to get clear visual field.
View Article and Find Full Text PDFDiabetes Metab Res Rev
September 2025
Department of Nephrology, Daping Hospital, Army Medical University, Chongqing, China.
Chronic kidney disease (CKD) substantially increases cardiovascular risk, with endothelial dysfunction as its central pathological mechanism. This review summarises the molecular regulatory mechanisms underlying endothelial dysfunction in CKD and highlights recent advances in treatment strategies. The pathophysiology of endothelial injuries involves a complex network of multiple factors and mechanisms, including oxidative stress, inflammation, glycocalyx damage, ischaemia, hypoxia, cellular senescence and endothelial-mesenchymal transition (EndMT).
View Article and Find Full Text PDFSTAR Protoc
September 2025
Division of Pulmonary Medicine and Critical Care, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Department of Systems Biology and Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA; Department of Pulmonary Medicine, Cincinnati Children's Hospital Medical C
Calcium signaling is crucial for endothelial cell homeostasis. Alterations in intracellular calcium levels due to shear stress are linked to vascular dysfunction and diseases. Here, we present a protocol to perform live calcium imaging by using a live calcium indicator on human lung endothelial cells subjected to shear stress in a commercially available microfluidic device (Ibidi Luer VI).
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