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Editorial
. 2017 Jun;31(3):229-232.
doi: 10.1007/s10557-017-6741-2.

Mechanistic Insights of Empagliflozin-Mediated Cardiac Benefits: Nearing the Starting Line : Editorial to: "Empagliflozin Improves Left Ventricular Diastolic Dysfunction in a Genetic Model of Type 2 Diabetes" by N. Hammoudi et al

Affiliations
Editorial

Mechanistic Insights of Empagliflozin-Mediated Cardiac Benefits: Nearing the Starting Line : Editorial to: "Empagliflozin Improves Left Ventricular Diastolic Dysfunction in a Genetic Model of Type 2 Diabetes" by N. Hammoudi et al

Manisha Gupte et al. Cardiovasc Drugs Ther. 2017 Jun.
No abstract available

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Conflict of interest statement

Conflict of Interest: All authors declared no conflict of interest.

Figures

Figure
Figure. Potential signaling mechanism for the beneficial effect of Empagliflozin (EMPA) on cardiac function
Multiple pathways have been implicated in the myocardial pathophysiology. Many of these diverse signaling cascades culminate into MAP kinases and AKT as the final effector molecule to modulate the gene program of cardiac remodeling and heart failure. The final effectors that are modulated by EMPA are shown. AKT, AKT8 virus oncogene cellular homolog; ECM, extracellular matrix; ERK, extracellular signal-regulated kinase; FAK, focal adhesion kinase; GPCR, G-protein coupled receptor; Grb2, growth factor receptor-bound protein 2; GRK2, G-protein coupled receptor kinase; ILK, integrin-linked kinase; IRS, insulin receptor substrate; JNK = Jun N-terminal kinase; MEK, MAPK/Erk kinase; PDK1, 3-phosphoinositide-dependent protein kinase 1; PI3K, phosphoinositide 3 kinase; PKA, protein kinase A; PLB, phospholamban; Rac1, Ras-related C3 botulinum toxin substrate 1; Raf, Rapidly Accelerated Fibrosarcoma; RhoA, Ras homolog gene family, member A; RTK, receptor tyrosine kinase; SERCA2a, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase; SOS, Son of sevenless guanine nucleotide exchange factor; TAK1, TGF β-activated kinase 1; TGFR, TGF-β1 receptor.

Comment on

References

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