Galectin-3 as a therapeutic target in pulmonary hypertension: Molecular mechanisms, drug development directions, and emerging clinical applications

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388971%3A_____%2F25%3A00642752" target="_blank" >RIV/61388971:_____/25:00642752 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985823:_____/25:00642752

Výsledek na webu

<a href="https://doi.org/10.1016/j.biopha.2025.118756" target="_blank" >https://doi.org/10.1016/j.biopha.2025.118756</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.biopha.2025.118756" target="_blank" >10.1016/j.biopha.2025.118756</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Galectin-3 as a therapeutic target in pulmonary hypertension: Molecular mechanisms, drug development directions, and emerging clinical applications

Popis výsledku v původním jazyce

Pulmonary hypertension (PH) remains a devastating cardiovascular disorder with limited targeted treatment. Galectin-3 has emerged as a promising therapeutic target due to its central role in vascular remodeling and inflammation. Galectin-3 exacerbates intimal hyperplasia by influencing endothelial cells through multiple mechanisms. It also contributes to medial hypertrophy and adventitial thickening by activating vascular smooth muscle cells and adventitial fibroblasts. In PH, right ventricular myocardium can be remodeled through galectin-3-mediated activation of cardiac fibroblasts and impaired cardiomyocyte contractility. Galectin-3 also modulates accompanying inflammatory reactions. This review explores the molecular mechanisms of galectin-3 action in PH and evaluates the potential of galectin-3 inhibition as a therapeutic strategy. Targeting galectin-3 represents a novel avenue in PH management but still faces challenges such as drug specificity and clinical efficacy. Future studies should focus on optimizing the structure and performance of galectin-3 inhibitors for clinical application.

Název v anglickém jazyce

Galectin-3 as a therapeutic target in pulmonary hypertension: Molecular mechanisms, drug development directions, and emerging clinical applications

Popis výsledku anglicky

Pulmonary hypertension (PH) remains a devastating cardiovascular disorder with limited targeted treatment. Galectin-3 has emerged as a promising therapeutic target due to its central role in vascular remodeling and inflammation. Galectin-3 exacerbates intimal hyperplasia by influencing endothelial cells through multiple mechanisms. It also contributes to medial hypertrophy and adventitial thickening by activating vascular smooth muscle cells and adventitial fibroblasts. In PH, right ventricular myocardium can be remodeled through galectin-3-mediated activation of cardiac fibroblasts and impaired cardiomyocyte contractility. Galectin-3 also modulates accompanying inflammatory reactions. This review explores the molecular mechanisms of galectin-3 action in PH and evaluates the potential of galectin-3 inhibition as a therapeutic strategy. Targeting galectin-3 represents a novel avenue in PH management but still faces challenges such as drug specificity and clinical efficacy. Future studies should focus on optimizing the structure and performance of galectin-3 inhibitors for clinical application.

Druh

J_SC - Článek v periodiku v databázi SCOPUS

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Biomedicine & Pharmacotherapy

ISSN

0753-3322

e-ISSN

1950-6007

Svazek periodika

193

Číslo periodika v rámci svazku

Dec

Stát vydavatele periodika

FR - Francouzská republika

Počet stran výsledku

21

Strana od-do

118756

Kód UT WoS článku

—

EID výsledku v databázi Scopus

2-s2.0-105021960356