CRP, or C-reactive protein, is a well-known acute-phase protein and a host-defense molecule conserved throughout evolution [1,2,3]. It can mediate phagocytosis initiation by labeling damaged cells, leading to the activation of the classical complement pathway (up to C4) and elimination of pathogens or damaged cells. CRP's binding to ligands like phosphocholine-modified substances and apoptotic cells masks their potentially harmful activities, and it also modulates complement activation, which is beneficial for the body [2]. CRP is a biomarker for inflammation, cardiovascular diseases, and certain cancers [4].

In the context of diseases, elevated CRP levels are associated with myocardial infarction, stroke, COVID-19, hypertension, and atherosclerotic plaque development [1,5]. For example, in "internal wounds" such as myocardial infarction and stroke, CRP can induce tissue damage to potentially regenerable tissue [1]. In COVID-19, CRP labels ischemic but potentially regenerable cells in the lungs [1]. In Nile tilapia, the CRP gene (On-CRP) promotes inflammation, activates the complement pathway, and improves phagocytic and bacterial agglutination activities during bacterial infection [6].

In conclusion, CRP is an evolutionarily conserved protein with important functions in host-defense, inflammation, and disease. Studies across different species and disease models, including those related to COVID-19, myocardial infarction, and hypertension, have revealed its diverse roles. Understanding CRP is crucial for further insights into disease mechanisms and potential therapeutic strategies.