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Respir Res
January 2025
Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 210011, Jiangsu Province, China.
Background: Sepsis is a systemic inflammatory response caused by infection. When this inflammatory response spreads to the lungs, it can lead to acute lung injury (ALI) or more severe acute respiratory distress syndrome (ARDS). Pulmonary fibrosis is a potential complication of these conditions, and the early occurrence of pulmonary fibrosis is associated with a higher mortality rate.
View Article and Find Full Text PDFCurr Med Sci
December 2024
Department of Cardiovasology, Affiliated Renhe Hospital of China Three Gorges University, Yichang, 443002, China.
Objective: To investigate whether cardiac mast cells (MCs) participate in pressure overload-induced myocardial hypertrophy through the regulation of transient receptor potential vanilloid 4 (TRPV4).
Methods: Pressure overload-induced myocardial hypertrophy was induced via abdominal aortic constriction (AAC). Myocardial hypertrophy was evaluated by measuring the heart weight index (HW/BW), lung weight index (LW/BW), ratio of heart weight to tibia length (HW/TL), ratio of lung weight to tibia length (LW/TL), and cross-sectional area of myocardial cells.
Bioorg Chem
December 2024
Department of Pharmacology, School of Life Sciences and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang 110016, China. Electronic address:
Oxidative stress has been confirmed to be closely related to the occurrence and development of pulmonary fibrosis (PF). The Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid-2 related factor 2 (Nrf2) pathway plays a key role in maintaining cellular redox homeostasis. Targeting the Keap1 protein to activate Nrf2 could be a promising strategy for treating PF.
View Article and Find Full Text PDFAm J Sports Med
November 2024
Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA.
Background: Injuries to the glenoid labrum have been recognized as a source of joint pain and discomfort, which may be associated with the inflammatory responses that lead to the deterioration of labral tissue. However, it is unclear whether the torn labrum prompts mast cell (MC) activation, resulting in synovial inflammatory responses that lead to labral tissue degeneration.
Purpose: To determine the potential influence of activated MC on synovial inflammatory responses and subsequent labral tissue degeneration and shoulder function deterioration in a rat model by monitoring MC behavior and sequential inflammatory responses within the synovial tissue and labral tissue after injury, suture repair, and MC stabilizer administration.
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