The molecular basis for cellular injury characteristic of cardiomyopathy associated with SCD. The figure illustrates the protective effects of 17R-RvD1 in mitigating key pathologic pathways. Inflammation regulation: 17R-RvD1 suppresses the activation of inflammatory pathways, including NF-κB signaling, by inhibiting the nuclear translocation of the NF-κB complex (p50/p65). It downregulates proinflammatory cytokines, such as IL-18 and IL-1β, through the modulation of the NLRP3 inflammasome. Antioxidant response: 17R-RvD1 enhances Nrf2 translocation, leading to increased expression of antioxidant proteins such as HO-1, SOD, and Cat, reducing oxidative stress in mitochondria and preventing the release of ROS and Cyto C. Fibrosis suppression: TGF-β/Smad2-3 signaling pathway, a critical driver of fibrosis, is attenuated by 17R-RvD1, resulting in reduced ECM protein production, fibrosis, and myofibroblast activation. Cyto C, cytochrome c; ER, endoplasmic reticulum; IL, interleukin; ROS, reactive oxygen species.