Hans J. Gabius

TL;DR: Galectin-3, a macrophage-derived mediator, induces cardiac fibroblast proliferation, collagen deposition, and ventricular dysfunction, which implies that HF therapy aimed at inflammatory responses may need to be targeted at the early stages of HF and probably needs to antagonize multiple inflammatory mediators, including galectIn-3.

TL;DR: Galectin-3 is unique among the Galectin family of animal lectins in its biological activities and structure as mentioned in this paper, it possesses anti-apoptotic activity and its kinetics of precipitation are fast, on the order of seconds.

TL;DR: It is concluded that Ac-SDKP prevents Gal-3-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction, possibly via inhibition of the TGF-beta/Smad3 signaling pathway.

TL;DR: The results demonstrated the candidacy of glycodendrimersomes as new mimics of biological membranes with programmable glycan ligand presentations, as supramolecular lectin blockers, vaccines, and targeted delivery devices.

TL;DR: The thermodynamics of binding of the multivalent carbohydrates to the C-terminal CRD domain of galectin-3 was shown to possess similar thermodynamic binding properties as the intact molecule, and the results have important implications for the design of carbohydrate inhibitors of the two galectins.