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. 2020 Jun 3;11:836. doi: 10.3389/fphar.2020.00836

Figure 2.

Figure 2

The MAPK pathway can be induced by several triggers in various cells within the context of CVDs. For example, pressure overload can cause hypertrophy in cardiomyocytes via the ERK1/2/GLUT pathway. Oxidized LDL triggers macrophage proliferation via ERK1/2/GM-CSF, which contributes to the development of atherosclerosis. All cells involved in atherosclerosis can release cytokines in an ERK1/2 dependent manner, which ultimately propel plaque and clot growth. Cytokines can subsequently enhance MMP9 production, which leads to plaque rupture and thrombosis. Meanwhile, coronaviruses have been shown to involve p38 MAPK, JNK, and MKK1/ERK1/2 pathways for viral pathogenesis. MKK1/ERK1/2 pathway also upregulates the protease furin, which is implicated in SARS-CoV-2 entry due to the unique furin-like S1/S2 cleavage site. It is worth examining if inhibition of MKK1/ERK1/2 mitigates production of SARS-CoV-2 viral progeny. On the other hand, SARS-CoV-2 can also amplify production of cytokines, which can worsen existing CVDs.