SARS-CoV2
infection not only causes abnormal severe
pneumonia but also induces other relevant pathophysiological effects on several tissues and organs. In this regard, the clinical complications observed in
COVID-19 include
acute coronary syndrome,
pulmonary thromboembolism,
myocarditis and, in the severe cases, the occurrence of
disseminated intravascular coagulation. Literature on
COVID-19 highlighted the central role of the Renin Angiotensin Aldosterone System in the determinism of SARS-CoV2 cellular internalization in the target tissues. Lung degeneration and respiratory distress appear to be dependent on the perturbance of physiological mechanisms, such as the uncontrolled release of pro-inflammatory
cytokines, a dysregulation of the fibrinolytic coagulative cascade and the hyperactivation of immune effector cells. In this mini review, we address the physiology of
Midkine, a
growth factor able to bind
heparin, and its pathophysiological potential role in
COVID-19 determinism.
Midkine increases in many inflammatory and autoimmune conditions and correlates with several dysfunctional immune-inflammatory responses that appear to show similarities with the pathophysiological elicited by SARS-CoV2.
Midkine, together with its receptor, could facilitate the virus entry, fostering its accumulation and increasing its affinity with Ace2 receptor. We also focus on Netosis, a particular mechanism of pathogen clearance exerted by neutrophils, which under certain pathological condition becomes dysfunctional and can cause tissue damage. Moreover, we highlight the mechanism of autophagy that the new coronavirus could try to escape in order to replicate itself, as well as on
pulmonary fibrosis induced by
hypoxia and on the release of
cytokines and
mediators of inflammation, correlating the interplay between
Midkine and SARS-CoV2.