Simultaneously, myoglobin-induced oxidative damage can increase the release of vasoconstrictors such as endothelin (ET), thromboxane A2 (TXA2), and tumor necrosis factor α (TNF-α) [17], as well as decrease the release of vasodilators such as NO [18], thereby aggravating renal vasoconstriction, reducing glomerular filtration rate, and causing AKI. Here, MB is linked to acute kidney injury.