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Thrombin generation and atherosclerosis

(2024) found that numerous mitochondrial function-related genes, including SQOR, were significantly upregulated in patients with steroid-induced osteonecrosis of the femoral head (SONFH), implicating mechanisms such as dysregulated mitochondrial apoptosis signaling (e.g., BCL-2 / BAX imbalance), increased oxidative stress, and altered energy metabolism

Its mechanism of action is mainly due to the nephrotoxic effect of contrast agents on renal tubules and vascular endothelial cells, which leads to hemodynamic changes, OS, apoptosis, and inflammatory reactions in the kidney

This meta-analysis concluded that there was insufficient evidence to recommend the routine use of inhaled steroids in adults with stable state BE but considered that a therapeutic trial might be justified in patients with difficult to control symptoms

Histopathological hallmarks include focal demyelinated lesions characterized by oligodendrocyte (OL) cell death, axonal damage, gliosis, microglial activation, and infiltration of lymphocytes and macrophages [1,2]