Myocardial Injury After Ischemia/Reperfusion Is Attenuated By Pharmacological Galectin-3 Inhibition

Ibarrola, Jaime; Matilla, Lara; Martínez‐Martínez, Ernesto; Gueret, A; Fernández‐Celis, Amaya; Henry, Jean‐Paul; Nicol, Lionel; Jaisser, Frédéric; Mulder, Paul; Ouvrard‐Pascaud, Antoine; López‐Andrés, Natalia

doi:10.1038/s41598-019-46119-6

Cited by 40 publications

(26 citation statements)

References 29 publications

(35 reference statements)

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“…Gal-3 inhibition by MCP is effective in decreasing both the ischemic area and the fibrotic remodeling in a rat model of ischemia/reperfusion [72]. Similarly, silencing of Gal-3 in cardiomyocytes isolated from rats and treated to simulate ischemia/reperfusion, resulted in a decreased apoptosis thanks to its interaction with bcl-2 [73].…”

Section: Gal-3 In Cardiac Fibrosis and Heart Failurementioning

confidence: 92%

Galectin-3 in Cardiovascular Diseases

Blanda

Bracale

Taranto

et al. 2020

IJMS

113

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Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis.

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Section: Gal-3 In Cardiac Fibrosis and Heart Failurementioning

confidence: 92%

Galectin-3 in Cardiovascular Diseases

Blanda

Bracale

Taranto

et al. 2020

IJMS

113

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“…5B). The decreased reperfusion contracture amplitude observed in intrinsic activity suggests that elevating [Na + ] o may mitigate ischemia and reperfusion injury, presumably by reducing the degree of intracellular Ca 2+ -overload [31][32][33][34][35] . With respect to the return of mechanical function, for both 145 and 155 mM Na + , the absolute LVDP during reperfusion was lower than during baseline, and paralleled the differences observed at baseline.…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Elevated perfusate [Na+] increases contractile dysfunction during ischemia and reperfusion

King

Padget

Perry

et al. 2020

Sci Rep

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Recent studies revealed that relatively small changes in perfusate sodium ([Na+]o) composition significantly affect cardiac electrical conduction and stability in contraction arrested ex vivo Langendorff heart preparations before and during simulated ischemia. Additionally, [Na+]o modulates cardiomyocyte contractility via a sodium-calcium exchanger (NCX) mediated pathway. It remains unknown, however, whether modest changes to [Na+]o that promote electrophysiologic stability similarly improve mechanical function during baseline and ischemia–reperfusion conditions. The purpose of this study was to quantify cardiac mechanical function during ischemia–reperfusion with perfusates containing 145 or 155 mM Na+ in Langendorff perfused isolated rat heart preparations. Relative to 145 mM Na+, perfusion with 155 mM [Na+]o decreased the amplitude of left-ventricular developed pressure (LVDP) at baseline and accelerated the onset of ischemic contracture. Inhibiting NCX with SEA0400 abolished LVDP depression caused by increasing [Na+]o at baseline and reduced the time to peak ischemic contracture. Ischemia–reperfusion decreased LVDP in all hearts with return of intrinsic activity, and reperfusion with 155 mM [Na+]o further depressed mechanical function. In summary, elevating [Na+]o by as little as 10 mM can significantly modulate mechanical function under baseline conditions, as well as during ischemia and reperfusion. Importantly, clinical use of Normal Saline, which contains 155 mM [Na+]o, with cardiac ischemia may require further investigation.

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“…Furthermore, MCP and perindopril comparably improved ischemic heart failure by downregulating Gal-3 and reducing myocardial fibrosis [20]. The blockade of Gal-3 with MCP prevented cardiac fibrosis, inflammation, and functional alterations [19].…”

Section: Fibrotic Diseasesmentioning

confidence: 99%

Pleiotropic Effects of Modified Citrus Pectin

Eliaz¹,

Raz

2019

Nutrients

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Modified citrus pectin (MCP) has a low-molecular-weight degree of esterification to allow absorption from the small intestinal epithelium into the circulation. MCP produces pleiotropic effects, including but not limited to its antagonism of galectin-3, which have shown benefit in preclinical and clinical models. Regarding cancer, MCP modulates several rate-limiting steps of the metastatic cascade. MCP can also affect cancer cell resistance to chemotherapy. Regarding fibrotic diseases, MCP modulates many of the steps involved in the pathogenesis of aortic stenosis. MCP also reduces fibrosis to the kidney, liver, and adipose tissue. Other benefits of MCP include detoxification and improved immune function. This review summarizes the pleiotropic effects of MCP.

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Myocardial Injury After Ischemia/Reperfusion Is Attenuated By Pharmacological Galectin-3 Inhibition

Cited by 40 publications

References 29 publications

Galectin-3 in Cardiovascular Diseases

Galectin-3 in Cardiovascular Diseases

Elevated perfusate [Na+] increases contractile dysfunction during ischemia and reperfusion

Pleiotropic Effects of Modified Citrus Pectin

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