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Updated: Jul 2, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Galectin-3, transforming growth factor beta 1, and brain natriuretic peptide in cardiac remodeling under

Hina Patel1, Angelie Pathak1, Resmi Rajalekshmi1

  • 1Department of Translational Research, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, 309 E. Second Street, Pomona, CA, 91766, USA.

Molecular and Cellular Biochemistry
|July 1, 2026
PubMed

Insights

Hyperlipidemia and hyperglycemia induce cardiac remodeling via distinct profibrotic signaling pathways. Galectin-3 and TGF-β1 may share a role in fibrosis, while BNP indicates a stress response in the heart.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Diseases
  • Molecular Cardiology

Background:

  • Hyperlipidemia (HYL) and hyperglycemia (HYG) are known drivers of pathological cardiac remodeling.
  • The precise mechanisms by which these metabolic conditions differentially regulate profibrotic signaling and stress-response pathways in the left ventricular (LV) myocardium are not fully understood.

Purpose of the Study:

  • To investigate the expression and localization of galectin-3 (Gal-3), transforming growth factor-β1 (TGF-β1), and brain natriuretic peptide (BNP) in the LV myocardium of a Yucatan miniswine model of HYL and HYG.
  • To elucidate the differential regulation of these key proteins under distinct metabolic insults.

Main Methods:

  • Yucatan miniswine were subjected to diets inducing HYL or HYG for 8 weeks.
  • Left ventricular (LV) tissues were analyzed using histology, quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry.

Main Results:

  • Both HYL and HYG induced cardiomyocyte hypertrophy and interstitial fibrosis, with HYG showing more diffuse collagen deposition.
  • Upregulation of Gal-3, TGF-β1, and BNP transcripts was observed, correlating positively with glucose levels.
  • Western blot revealed greater active TGF-β1 in HYL and precursor accumulation in HYG, indicating condition-specific TGF-β1 regulation.
  • Immunohistochemistry showed distinct localization patterns for Gal-3 (perivascular), TGF-β1 (cardiomyocyte cytoplasm/perinucleus), and BNP (Purkinje fibers), with increased staining in stressed groups.

Conclusions:

  • HYL and HYG are associated with overlapping yet distinct patterns of Gal-3, TGF-β1, and BNP expression during cardiac remodeling.
  • The Gal-3/TGF-β1 axis may represent a common profibrotic pathway in metabolic cardiac remodeling.
  • BNP expression suggests a compensatory stress response, warranting further mechanistic investigation.

Keywords:
Brain natriuretic peptideCardiac remodelingCardiomyopathyFibrosisGalectin-3/TGF-β1 signalingHyperglycemiaHyperlipidemiaMetabolic cardiomyopathyPathologic cardiac hypertrophy

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