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ERR in particular is highly expressed in tissues with high energy demands, including heart, skeletal muscle, brown adipose tissue, and kidney, where it coordinates the expression of metabolic gene networks

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However, unlike previous findings, shikonin, icariin, and other drugs induce mitochondrial dysfunction by increasing ROS levels, decreasing mitochondrial membrane potential, and elevating the release of cytochrome C and pro-apoptotic proteins, such as caspase-3 and caspase-9, to induce apoptosis in FLSs to suppress inflammatory response (265, 266)

However, further research is needed to determine the intermediate level of its concentration [23]