Galectins-A Potential Target for Cardiovascular Therapy.
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.
King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah 21589. Saudi Arabia.
Ghulam Md
GM
Ashraf
Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, Uttar Pradesh. India.
Asma
A
Perveen
Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah. Saudi Arabia.
Syed Kashif
SK
Zaidi
Amity Institute of Biotechnology, Amity University Uttar Pradesh, Lucknow, Uttar Pradesh. India.
Ausaf
A
Ahmad
Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah. Saudi Arabia.
Shazi
S
Shakil
King Fahd Medical Research Center, King Abdulaziz University, Jeddah. Saudi Arabia.
Chelapram Kandy
CK
Firoz
King Fahd Medical Research Center, King Abdulaziz University, Jeddah. Saudi Arabia.
Nasimudeen R
NR
Jabir
Department of Zoology, College of Sciences, King Saud University, Riyadh. Saudi Arabia.
Iftekhar
I
Hassan
Applied Biotechnology Department, Sur College of Applied Sciences, Sur. Oman.
Taqi Ahmad
TA
Khan
Department of Biochemistry and Bioinformatics, Institute of Science, GITAM University, Vishakhapatnam-530045, A.P. India.
Nagendra Sastry
NS
Yarla
King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah 21589. Saudi Arabia.
Shams
S
Tabrez
D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000503:physiopathology*; D037161:Galectins / Q000187:drug effects* / Q000502:physiology*; D006801:Humans; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000503:physiopathology; D018919:Neovascularization, Physiologic / Q000187:drug effects
D037161:Galectins
Angiogenesis; atherosclerosis; cardiovascular disease; galectin; therapy