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. 2021 Nov 15;22(22):12326. doi: 10.3390/ijms222212326

Figure 2.

Figure 2

Schematic model representing the cellular localization, the molecular mechanisms and the effects of PPARs activation after cerebral and cardiac ischemia. Under unliganded state, monomer or dimer of PPAR is bound to multicomponent repressors (1). Ligand-dependent transactivation: ligand binding to either PPAR or RXR causes displacement of bound repressors, recruitment of co-activators and activation of gene transcription (2). Ligand-independent repression: PPARs bind to response elements in the absence of ligand and recruit multicomponent repressors that mediate active repression (3). Ligand-dependent repression is provided by several mechanisms: competition for a limiting pool of co-activators (4), inhibition of repressors clearance (5), direct interaction with other transcription factors (e.g., p65/p50) (6,7). Finally, several kinases can phosphorylate PPARs modulating its activity (e.g., PPAR-mediated transcription is increased by PKA, while is reduced by MAPK and Brc kinase) (8). ° the expression is increased after MI; * the expression is increased after LPS treatment.