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Vascular calcification (VC) was defined as the ectopic deposition of calcium-phosphorus complexes on the blood vessel walls. It was a process involving multiple factors and mechanisms, covering the phenotype transition of vascular smooth muscle cells (VSMCs) and release of microvesicles. It was a common end-stage alteration of chronic diseases such as cardiovascular disease and chronic kidney disease. Increasing evidence indicates that mitochondria were involved in the development of VC. Mitochondria provided energy to cells, maintained the stability of cell functions, and participated in a variety of biological behavior. Oxidative stress, autophagy, apoptosis, and mitochondrial DNA (mtDNA) damage could affect the development of VSMCs calcification by alteration of mitochondrial function. This article reviewed the mechanism of calcification and the role of mitochondria in VC, aiming to raise a novel insight into drug development and clinical treatment.
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http://dx.doi.org/10.2478/jtim-2020-0013 | DOI Listing |
Cell Signal
March 2025
Department of Urology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, People's Republic of China. Electronic address:
Succinylation is a relatively common post-translational modification. It occurs in the cytoplasm, mitochondria, and the nucleus, where its essential precursor, succinyl-CoA, is present, allowing for the modification of non-histone and histone proteins. In normal cells, succinylation levels are carefully regulated to sustain a dynamic balance, necessitating the involvement of various regulatory mechanisms, including non-enzymatic reactions, succinyltransferases, and desuccinylases.
View Article and Find Full Text PDFEur J Pharmacol
March 2025
Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, AlBeheira, Egypt. Electronic address:
Humanin (HN) is an endogenous micropeptide also known as a mitochondria-derived peptide. It has a neuroprotective effect against Alzheimer's disease (AD) and other neurodegenerative diseases by improving hippocampal acetylcholine and attenuating the development of oxidative stress and associated neurotoxicity. HN protects the neuron from the toxic effects of amyloid beta (Aβ).
View Article and Find Full Text PDFExp Neurol
March 2025
Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China. Electronic address:
Mitochondrial autophagy (mitophagy) plays an essential role in the maintenance of mitochondrial homeostasis. Defective mitophagy triggered by amyloid beta (Aβ) is linked to neuronal deterioration and neurodegeneration in Alzheimer's disease (AD). However, the molecular mechanism underlying the defective mitophagy in AD is still not fully illustrated.
View Article and Find Full Text PDFBMC Pregnancy Childbirth
March 2025
Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
Background: Gestational diabetes mellitus (GDM) affects up to 14% of pregnancies globally, with insulin resistance (IR) playing a critical but often underappreciated role in its pathogenesis. Yet the specific impact of insulin at IR levels on mitochondrial function and pyroptosis in first-trimester trophoblasts remains unclear. Metformin use in GDM pregnancies is rising, but its impact on placental mitochondrial function is uncertain.
View Article and Find Full Text PDFCell Death Dis
March 2025
National Clinical Research Center for Digestive Diseases, Department of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Mitochondrial dysfunction contributes to the pathogenesis of ulcerative colitis (UC). As a mitochondrial isozyme of creatine kinases, which control energy metabolism, CKMT1 is thought to be a critical molecule in biological processes. However, the specific role of CKMT1 in intestinal inflammation remains largely unknown.
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