A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

Figure 3

Schematic overview of the relationship between PPAR-response elements (PPREs) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) in cardiac remodelling. AKT: protein kinase B; AMPK: adenosine monophosphate-activated protein kinase; ERK1/2: extracellular signal-regulated kinase 1/2; ERR: estrogen-related receptor; GPCR: G-protein coupled receptor; GSK3β: glycogen synthase kinase 3 beta; IKK: IκB kinase; IκB: inhibitor of NF-κB; INSR: insulin receptor; IRS: insulin receptor substrate; LATS 1/2: serine/threonine-protein kinase 1/22; LKB1: liver kinase B1; MEK: mitogen-activated protein kinase kinase; MSK1: mitogen and stress-related kinase 1; MST1: mammalian sterile 20-like kinase; mTORC: mammalian target of rapamycin complex 1 and mTORC-2; ORAI1/3: calcium release-activated calcium channel protein 1/3; PDC: pyruvate dehydrogenase complex; PDK4: pyruvate dehydrogenase kinase; PDP1: pyruvate dehydrogenase phosphatase1; PI3K: phosphoinositide 3 kinase; PI3K: phosphoinositide 3-kinase; RAF: serine/threonine-specific protein kinases; RAS: small GTPase RAS; RHEB: RAS homolog enriched in brain; RXR: 9-cis-retinoic acid receptor; S6 K1: S6 kinase 1; STIM-1: stromal interaction molecule-1; TSC-1/2: tuberous sclerosis- 1/2; YAP: yes-associated protein. See text for details. The figure was made in part using tools provided by Servier Medical Arts.