The role of Heme oxygenase-1 (HO-1) in sepsis-associated organ damage: A systematic review.

Sepsis-induced myopathy is a significant cause of intensive care unit-acquired weakness (ICUAW) and a leading cause of mortality in ICU patients. ICUAW primarily affects the respiratory muscles and limb skeletal muscles, leading to prolonged mechanical ventilation and bedridden periods. This condition increases the risk of complications such as pneumonia, atelectasis, and lower extremity venous thrombosis, thereby impacting patients' quality of life and, in severe cases, jeopardizing their lives. The pathogenesis of sepsis-induced myopathy is complex, and currently, there are no effective preventive or therapeutic measures available. Heme oxygenase-1 (HO-1) catalyzes the metabolism of heme, resulting in the production of carbon monoxide (CO), biliverdin, and ferritin. It possesses anti-inflammatory, antioxidant stress response, anti-apoptotic, and tissue perfusion improvement functions. Studies have demonstrated a correlation between HO-1 and the occurrence and progression of multiple organ dysfunction syndrome in sepsis, as well as its ability to ameliorate skeletal muscle dysfunction caused by various diseases. Based on the existing literature on HO-1, sepsis, and skeletal muscle myopathy, this review aims to explore the potential mechanisms and therapeutic potential of HO-1 in the treatment of sepsis-induced myopathy.