Abstract
Cells constantly adapt to external humoral cues like cytokines and hormones, but practically most cellular behavior is under locally guided control via cell–cell interactions. Galectins (Gals) are one of the most prominent members of the group of molecules involved in this intercellular signaling. They are the family of β-galactoside specific lectins and consist of 15 different types, each with a specific function. They play crucial role in the immune system, inflammation, wound healing and carcinogenesis. In recent times, the role of Gals in the development of cardiovascular disease (CVD) has gained attention. Gals have been reported to act ambiguously by both relieving ischemia and accelerating atherosclerosis. Atherosclerosis can ultimately lead to myocardial infarction or ischemic stroke, which are both associated with Gals. There is also a role for Gals in the development of myocarditis by their influence on inflammatory processes. Moreover, Gal acts as a biomarker for the severity of myocardial ischemia and heart failure (HF). This review summarizes the association between Gals and the development and pathogenesis of CVD like atherosclerosis, stroke, myocardial infarction, and HF. A comprehensive outline of the association between Gals and more general mechanisms such as angiogenesis, arteriogenesis and atherosclerosis has also been provided. Modulation of Gal signaling holds great promise for the treatment of CVD as evident from preclinical studies.
Keywords: Angiogenesis, atherosclerosis, cardiovascular disease, galectin, therapy.
Current Vascular Pharmacology
Title:Galectins-A Potential Target for Cardiovascular Therapy
Volume: 15 Issue: 4
Author(s): Ghulam Md. Ashraf*, Asma Perveen, Syed Kashif Zaidi, Ausaf Ahmad, Shazi Shakil, Chelapram Kandy Firoz, Nasimudeen R. Jabir, Iftekhar Hassan, Taqi Ahmad Khan, Nagendra Sastry Yarla and Shams Tabrez*
Affiliation:
- King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah 21589,Saudi Arabia
- King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah 21589,Saudi Arabia
Keywords: Angiogenesis, atherosclerosis, cardiovascular disease, galectin, therapy.
Abstract: Cells constantly adapt to external humoral cues like cytokines and hormones, but practically most cellular behavior is under locally guided control via cell–cell interactions. Galectins (Gals) are one of the most prominent members of the group of molecules involved in this intercellular signaling. They are the family of β-galactoside specific lectins and consist of 15 different types, each with a specific function. They play crucial role in the immune system, inflammation, wound healing and carcinogenesis. In recent times, the role of Gals in the development of cardiovascular disease (CVD) has gained attention. Gals have been reported to act ambiguously by both relieving ischemia and accelerating atherosclerosis. Atherosclerosis can ultimately lead to myocardial infarction or ischemic stroke, which are both associated with Gals. There is also a role for Gals in the development of myocarditis by their influence on inflammatory processes. Moreover, Gal acts as a biomarker for the severity of myocardial ischemia and heart failure (HF). This review summarizes the association between Gals and the development and pathogenesis of CVD like atherosclerosis, stroke, myocardial infarction, and HF. A comprehensive outline of the association between Gals and more general mechanisms such as angiogenesis, arteriogenesis and atherosclerosis has also been provided. Modulation of Gal signaling holds great promise for the treatment of CVD as evident from preclinical studies.
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Cite this article as:
Md. Ashraf Ghulam *, Perveen Asma , Zaidi Kashif Syed , Ahmad Ausaf , Shakil Shazi , Firoz Kandy Chelapram , Jabir R. Nasimudeen , Hassan Iftekhar , Khan Ahmad Taqi , Yarla Sastry Nagendra and Tabrez Shams *, Galectins-A Potential Target for Cardiovascular Therapy, Current Vascular Pharmacology 2017; 15 (4) . https://dx.doi.org/10.2174/1570161115666170201113046
DOI https://dx.doi.org/10.2174/1570161115666170201113046 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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