## 4 Discussion
MPO is crucial for the oxidative burst, generating ROS [64; 65]. During MI, excessive MPO release can exacerbate oxidative stress within the cardiac tissue, leading to further cellular damage and initiating inflammatory responses. This oxidative stress is intimately linked to forming AOPP, primarily through the action of hypochlorous acid (HOCI) produced by MPO [66; 67]. Our in vitro studies using human serum albumin (HSA) demonstrated that chloramine T, a source of active chlorine substituting unstable HOCI, induces the formation of AOPP-HSA in a dose-dependent exponential manner [68]. It is important to note that the breakdown of extracellular DNA, particularly mitochondrial DNA (mtDNA) released during necrotic and apoptotic cell processes and DNA liberated during the formation of NETs, can contribute to an increase in serum uric acid levels [69]. While this correlation suggests an essential intersection between cellular death processes and metabolic alterations after cardiac injury, the exact mechanisms by which mtDNA from necrotic cells influences uric acid levels are not fully understood. Continued research in this domain may reveal crucial insights into the metabolic and cellular responses activated during myocardial infarction and other forms of cardiac stress. One study has posited that uric acid may promote myocardial infarction injury by activating specific inflammatory pathways [70]. Hence, the reactions leading to AOPP formation and increased serum uric acid might establish a feedback loop, intensifying cardiac damage and complicating the inflammatory response. In summary, the relationship between extracellular DNA, serum uric acid, AOPP formation, and oxidative stress appears to form a complex network of responses following cardiac injury. This interconnectedness highlights the complexity of the immune response to cardiac tissue damage and its implications for inflammation and oxidative stress in the context of MI, as suggested by this hypothesis. The increase in AOPP in this clinical situation may also be related to the mechanism of cardiomyocyte ischemia. During myocardial ischemia, oxygen supply to the heart muscle is significantly reduced or completely cut off due to blocked or narrowed coronary arteries [71]. Without sufficient oxygen, cardiac myocytes switch from aerobic metabolism, which utilizes oxygen, to anaerobic glycolysis, a less efficient form of energy production. Hypoxia-inducible factors (HIFs) are crucial in cellular responses to low oxygen levels during myocardial ischemia and reperfusion injury where HIF-1 alfa, a specific isoform of HIF, exerts a notable influence on neutrophil function, significantly impacting inflammation and tissue damage [72; 73]. HIF-1 alfa's role in modulating neutrophil function is noteworthy because it can potentially prolong the lifespan of neutrophils by affecting apoptosis (programmed cell death) and cell survival pathways [74]. This can lead to an increased number of neutrophils in the affected tissue. Consequently, the elevated presence of neutrophils, which are closely associated with inflammation and immune responses, may contribute to the rise of AOPP. Some studies suggest that the accumulation of AOPP may accelerate the progression of chronic kidney disease [75; 76]. It has been shown that an increase in plasma AOPP levels in the remnant kidney model leads to kidney damage. This is manifested by increased tubular fibrosis and glomerulosclerosis, worsening proteinuria, and overall deterioration of renal function [75]. Furthermore, one study suggests that AOPP may disrupt the process of autophagy in renal tubular epithelial cells (RTECs) by activating the PI3K/AKT/mTOR signaling pathway. This inhibition of autophagy plays a significant role in AOPP-induced RTEC injury, potentially contributing to the deterioration of kidney function and the development of kidney diseases [76]. Consequently, uric acid levels may also rise due to impaired renal function, as the kidneys cannot excrete uric acid effectively.