# Computational Assessment of Galectin-3 Significance in Heart Failure Remodeling

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 2020 · $675,768

## Abstract

Project Summary
Heart failure is a major growing public health problem with high morbidity and mortality.
Despite extensive research and advances in drug development, there is still a strong
demand for novel pharmacological agents that attenuate or reverse cardiac remodeling
and prevent heart failure. Inflammatory mechanisms including macrophage activation
and tissue fibrosis have been proposed to play an important role in cardiac remodeling
and progression of heart failure. Interstitial fibrosis of viable myocardium following
cardiac injury or pressure overload impairs tissue structure and behavior. Cells that are
contributing to fibrosis of myocardium are primarily fibroblast and myofibroblats, which
are phenotypically transformed fibroblast-like cells. Galectin-3 (a small protein) is
emerging as a key player with a substantial role in the process of heart failure. It has
been speculated that Galectin-3 promotes heart failure through involvement of multiple
mechanisms including cardiac fibroblast proliferation, collagen deposition, and
development of fibrosis. Excess collagen can potentially disturb extracellular matrix
environment (ECM) resulting in alteration of spatial configuration of cardiac muscle fibers
with respect to adjacent muscle elements. Alteration of muscle fiber configuration
perturbs the cardiac clockwise and anticlockwise torsion, which is essential for normal
pump function. Moreover, increase in myocardial collagen content could alter ventricular
filling properties particularly by increasing diastolic stiffness. Clearly, an accurate
assessment of left ventricular structure and function is an essential step to evaluate role
of Galectin-3 inhibition in attenuating/reversing cardiac remodeling. In this study,
sophisticated mathematical tools will be applied to in-vivo and ex-vivo cardiac images to
identify correlation between Galectin-3 deletion and cardiac remodeling using two
common murine models of heart failure (myocardial infarction and transverse aortic
constriction). Immunohistochemistry techniques will be also used to evaluate Galectin-3
expression, presence of inflammatory cells (macrophages, fibroblasts and
myofibroblasts), and tissue fibrosis in myocardial tissues. Outcome of this study provides
novel mechanistic information that can guide the development of next generation
therapeutic drugs targeting post-infarction and post-stress inflammatory response.

## Key facts

- **NIH application ID:** 9922954
- **Project number:** 5R01HL130292-04
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Siamak Ardekani
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $675,768
- **Award type:** 5
- **Project period:** 2016-07-01 → 2023-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9922954

## Citation

> US National Institutes of Health, RePORTER application 9922954, Computational Assessment of Galectin-3 Significance in Heart Failure Remodeling (5R01HL130292-04). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9922954. Licensed CC0.

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