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Gene Transfer for Ischemic Heart Failure in a Preclinical Model
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Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage

Alex Ali Sayour1, Attila Oláh2, Mihály Ruppert2

  • 1Experimental Research Laboratory, Heart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122, Budapest, Hungary. alexali.sayour@gmail.com.

Cardiovascular Diabetology
|October 1, 2020
PubMed
Abstract

Insights

Left ventricular SGLT1 is upregulated in heart failure, correlating with cardiac remodeling and function. Cardiac resynchronization therapy downregulates SGLT1 in dilated cardiomyopathy patients, suggesting a role in heart failure progression.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Selective SGLT2 inhibitors offer cardiovascular protection, but dual SGLT1/2 inhibitors' effects are less understood.
  • Left ventricular SGLT1 expression in various heart failure (HF) types is not well-characterized.
  • Understanding glucose transporter expression is crucial for novel therapeutic strategies in HF.

Purpose of the Study:

  • To investigate left ventricular (LV) SGLT1 expression in end-stage human heart failure.
  • To compare LV SGLT1 expression across different HF etiologies (HCM, DCM, IHD).
  • To explore the relationship between LV SGLT1, cardiac remodeling, systolic function, and therapeutic interventions like CRT.

Main Methods:

  • Gene and protein expression analysis of SGLT1, GLUT1, and GLUT4 in LV samples from HF patients and controls.
  • Quantification of SGLT1 protein, AMPKα, and ERK1/2 phosphorylation via Western blotting.
  • Immunohistochemical staining to localize SGLT1 expression within the myocardium.

Main Results:

  • LV SGLT1 mRNA and protein were significantly upregulated in DCM, IHD, and IHD+T2DM HF patients compared to controls, but not in HCM.
  • SGLT1 expression positively correlated with LV end-diastolic diameter (LVEDD) and negatively with ejection fraction (EF).
  • SGLT1 upregulation was linked to AMPKα phosphorylation and inversely associated with ERK1/2 phosphorylation; SGLT1 localized to cardiomyocytes.

Conclusions:

  • Myocardial LV SGLT1 is upregulated in most HF types, correlating with adverse cardiac remodeling and impaired systolic function.
  • Cardiac resynchronization therapy (CRT) reduced LV SGLT1 expression, particularly in DCM patients.
  • Further research is needed to elucidate the role of SGLT1 in LV remodeling and its therapeutic potential in heart failure.
Keywords:
Cardiac resynchronization therapyDual SGLT1/2 inhibitorsHeart failureSGLT2 inhibitorSodium-glucose cotransporter 1

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