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Cardioprotective effects of galectin-3 inhibition against ischemia/reperfusion injury
Dan Mo1, Wen Tian1, Hui-Nan Zhang1
1Key Laboratory of Gastrointestinal Pharmacology of Chinese Materia Medica of the State Administration of Traditional Chinese Medicine, Department of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an, China.
Insights
Galectin-3 inhibition protects the heart from injury caused by restoring blood flow after ischemia. Blocking galectin-3 reduces heart damage, apoptosis, and improves cardiac function, showing therapeutic potential.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Myocardial ischemia/reperfusion (IR) injury is a significant clinical problem.
- Galectin-3 is implicated as a biomarker in heart disease, but its role in IR injury is not fully understood.
Purpose of the Study:
- To investigate the role of galectin-3 in myocardial IR injury.
- To determine if inhibiting galectin-3 can protect the heart from IR-induced damage.
Main Methods:
- RNA sequencing (RNA-seq) to identify Lgals3 involvement.
- In vivo and in vitro assays (immunostaining, immunoblot) to assess galectin-3 expression.
- Echocardiography and infarct size analysis in galectin-3 inhibitor-treated mice.
- TUNEL staining, mitochondrial membrane potential (MMP), and mitochondrial permeability transition pore (mPTP) assessments.
Main Results:
- Lgals3 expression was significantly upregulated in myocardial IR injury.
- Treatment with galectin-3 inhibitors (pectin, G3-C12) attenuated cardiac dysfunction and reduced infarct size.
- Galectin-3 inhibition suppressed cardiomyocyte apoptosis and preserved mitochondrial function.
Conclusions:
- Pathological upregulation of galectin-3 contributes to IR-induced cardiac dysfunction.
- Galectin-3 inhibition ameliorates myocardial IR injury, suggesting therapeutic potential for heart protection.
Abstract:
Myocardial ischemia/reperfusion (IR) injury is caused by the restoration of the coronary blood flow following an ischemic episode. Accumulating evidence suggests that galectin-3, a β-galactoside-binding lectin, acts as a biomarker in heart disease. However, it remains unclear whether manipulating galectin-3 affects the susceptibility of the heart to IR injury. In this study, RNA sequencing (RNA-seq) analysis identified that Lgals3 (galecin-3) plays an indispensable role in IR-induced cardiac damage. Immunostaining and immunoblot assays confirmed that the expression of galectin-3 was markedly increased in myocardial IR injury both in vivo and in vitro. Echocardiographic analysis showed that cardiac dysfunction in experimental IR injury was significantly attenuated by galectin-3 inhibitors including pectin (1%, i.p.) from citrus and binding peptide G3-C12 (5.0 mg/kg, i.p.). Galectin-3 inhibitor-treated mice exhibited smaller infarct sizes and decreased tissue injury. Furthermore, TUNEL staining showed that galectin-3 inhibition suppressed IR-mediated cardiomyocyte apoptosis. Mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (mPTP) levels were well-preserved and IR-induced changes of mitochondrial cyto c, cytosol cyto c, caspase-9, caspase-3, Bcl-2 and Bax in the galectin-3 inhibitor-treated groups were observed. Our findings indicate that the pathological upregulation of galectin-3 contributes to IR-induced cardiac dysfunction and that galectin-3 inhibition ameliorates myocardial injury, highlighting its therapeutic potential.
