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Androgenic Anabolic Steroids Cause Thiol Imbalance in the Vascular Endothelial Cells.
Front Biosci (Landmark Ed)
January 2025
Department of Cytobiology and Proteomics, Medical University of Lodz, 92-215 Lodz, Poland.
Background: Androgenic anabolic steroids (AASs) are synthetic drugs structurally related to testosterone, with the ability to bind to androgen receptors. Their uncontrolled use by professional and recreational sportspeople is a widespread problem. AAS abuse is correlated with severe damage to the cardiovascular system, including changes in homeostasis and coagulation disorders.
View Article and Find Full Text PDFEmerging Pharmacological Interventions for Chronic Venous Insufficiency: A Comprehensive Systematic Review and Meta-Analysis of Efficacy, Safety, and Therapeutic Advances.
Pharmaceutics
January 2025
Multidisciplinary Laboratory of Scientific Evidence, University Center of Mineiros (Unifimes), Mineiros 75833-130, GO, Brazil.
Chronic Venous Insufficiency (CVI) is a progressive vascular condition characterized by venous hypertension and chronic inflammation, leading to significant clinical and socioeconomic impacts. This study aimed to evaluate the efficacy and safety of emerging pharmacological interventions for CVI, focusing on clinical outcomes such as pain, edema, cutaneous blood flow, and quality of life. Eligible interventions comprised new vasoprotective drugs, such as hydroxyethylrutoside, Pycnogenol, aminaphthone, coumarin + troxerutin, and Venoruton, compared to the standard therapy of diosmin and hesperidin.
View Article and Find Full Text PDFDysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases.
Pharmaceuticals (Basel)
January 2025
Department of Cardiac Surgery, Michigan Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Mitochondria dysfunction plays a central role in the development of vascular diseases as oxidative stress promotes alterations in mitochondrial morphology and function that contribute to disease progression. Redox imbalances can affect normal cellular processes including mitochondrial biogenesis, electrochemical equilibrium, and the regulation of mitochondrial DNA. In this review, we will discuss these imbalances and, in particular, the potential role of mitochondrial fusion, fission, biogenesis, and mitophagy in the context of vascular diseases and how the dysregulation of normal function might contribute to disease progression.
View Article and Find Full Text PDFLong-Term Oro-Dental Effects of Chemotherapy in a Pediatric Patient: A Case Study and a Proposed Oral Care Protocol.
J Clin Med
January 2025
Department of Oral Biology, Faculty of Dentistry, Naresuan University, Phitsanulok 65000, Thailand.
: Chemotherapy (CMT) in children can disrupt dental development and calcification, causing long-term dental issues, but good dental care and habits can help improve quality of life. This case report examines permanent dental disturbances in a 7-year, 4-month-old girl undergoing CMT, explores the histology of microdontia, and outlines an oral treatment plan for CMT management. : Clinical examination revealed microdontia and a groove crossing the cervical area (chronological hypoplasia), which were assessed using panoramic radiographs and histological analysis.
View Article and Find Full Text PDFPathophysiology of Group 3 Pulmonary Hypertension Associated with Lung Diseases and/or Hypoxia.
Int J Mol Sci
January 2025
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Pulmonary hypertension associated with lung diseases and/or hypoxia is classified as group 3 in the clinical classification of pulmonary hypertension. The efficacy of existing selective pulmonary vasodilators for group 3 pulmonary hypertension is still unknown, and it is currently associated with a poor prognosis. The mechanisms by which pulmonary hypertension occurs include hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, a decrease in pulmonary vascular beds, endothelial dysfunction, endothelial-to-mesenchymal transition, mitochondrial dysfunction, oxidative stress, hypoxia-inducible factors (HIFs), inflammation, microRNA, and genetic predisposition.
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