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. 2013 Jan 16;8(1):e54054. doi: 10.1371/journal.pone.0054054

Figure 6. Graphical illustration summarizing the proposed mechanism underlying TWEAK-induced cardiac dysfunction.

Figure 6

Normal PGC1 levels maintain OXPHOS gene expression and mitochodrial function to support cardiomyocyte contractility (left panel). TWEAK downregulates PGC1 levels through FN14-TRAF2-NFκB-dependent signaling, leading to impaired OXPHOS gene expression and mitochondrial dysfunction, and reduced cardiomyocyte contractility (right panel).