Figure and Table legends
Fig. 1. Signaling pathways and molecules related to physiological and
pathological cardiac hypertrophy (Modified
from[2]).
4E-BP1, eukaryotic translation initiation factor 4E-binding protein 1;
Akt1, protein kinase B; AT1-R, angiotensin II receptor;
β-AR, β-adrenergic receptor; C/EBPβ, CCAAT/enhancer-binding protein b;
CITED4, CBP/p300-interacting transactivator 4; DAG, diacylglycerol; ET 1
endothelin-1; ET-R, endothelin receptor; IP3, inositol trisphosphate;
IP3R, inositol triphosphate receptor; NE, noradrenaline; PKA, protein
kinase A; PKC, protein kinase C; PKD, protein kinase D; PKG, protein
kinase G; PLC, phospholipase C; PRAS40, proline-rich AKT substrate;
S6K1, ribosomal protein s6 kinase 1; SRF, serum response factor; Raf1,
RAF proto-oncogene serine/threonine-protein kinase; HDACs, histone
deacetylases; IGF-1, Insulin-like growth factor-1; PI3K,
phosphoinositide 3-kinase; Akt, protein kinase B; AMPK, AMP-activated
protein kinase; mTOR, mammalian target of rapamycin; MEK, MAP kinase
kinase; ERK, extracellular signal-related kinase; NFAT, nuclear factors
of activated T cell; CaMKII, Ca2+-regulated
calmodulin-dependent kinase II; NO, Nitric oxide; cGMP, 3’,5’-Cyclic
guanosine monophosphate; GC, guanylate cyclase; RHOA, transforming
protein RHOA; TRPC, transient receptor potential channel; IRS1/2,
insulin receptor substrate proteins 1 and 2.
Fig. 2. Roles of autophagy in cardiac hypertrophy.
Atg5, autophagy-related 5; Atg7, autophagy-related 7; NLRC5,
nucleotide-binding oligomerization domain (NOD)-like receptor family
CARD domain containing 5; HDAC, histone deacetylases; MSTN, myostatin.
Table 1 The potential autophagy modulators for treating pathological
cardiac hypertrophy.