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.