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. Author manuscript; available in PMC: 2012 Jun 12.
Published in final edited form as: Trends Cardiovasc Med. 2011 May;21(4):124–127. doi: 10.1016/j.tcm.2012.03.010

Figure 1.

Figure 1

Nutrient deprivation or other forms of environmental stress result in increased intracellular AMP levels and activation of AMPK. AMPK increases protein degradation via several different mechanisms, including autophagy and proteasome-mediated protein degradation by upregulating ubiquitin ligases. Specifically, AMPK regulates MuRF1 expression through the transcription factor MEF2, and regulates Atrogin-1 expression through an as yet unknown mechanism. During starvation, MuRF1 degrades myosin binding protein C and troponin I, which may contribute to decreased cardiac function. MuRF1 also degrades metabolic enzymes like aldolase a and pyruvate dehydrogenase (not shown in the figure). Hence, protein degradation is a mediator of cardiomyocyte remodeling, particularly during metabolic stress in the cardiomyocyte. See text for details. Dashed lines refer to possible crosstalk or as yet unknown mechanisms.