Table 1.

Proven roles of galectin-3 in bone biology and supposed functions, to be investigated, in the pathophysiology of bone metabolism.

Cell	Proven	To Be Investigated
Chondrocyte	cell marker and pro-survival factor [1,36] regulator of cell-to-cell interaction with chondroclasts [37] target and regulator of MMPs activity [38,39,40]	mechanisms underlying the regulation of chondrocyte activity and survival
Osteoblast	RUNX2 target gene [32] differentiation marker [41] proper bone ECM structure by regulating collagen fibers synthesis [42] protection against AGE mediated toxic effects by its AGE-receptor scavenger activity [43,44,45]	mechanisms underlying the regulation of osteoblast differentiationprotection from age- and diabetes-related bone fragility
Osteocyte	cell marker [1,41]	mechanosensory function and promotion of bone modelling and remodeling
MSC	increased osteoblastogenic differentiation capacity [46] positive regulation of the master transcription factor RUNX2 [46] stabilization and increase of β-catenin levels [46]	promotion of bone repair and homeostasis through modulation of β-catenin
Osteoclast	differentiation marker [47] mediator of cell matrix adhesion [48] regulation of differentiation from progenitors and pro-survival factor [40] downstream regulator of MMP-9 activity [40] and ECM degradation [37] negative regulation of osteoclastogenesis [49,50]	opposite effects depending on intra- and extracellular localization

MMPs = matrix metalloproteinases; RUNX2 = Runt-related transcription factor 2; ECM = extracellular matrix; AGEs = advanced glycation endproducts.