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Angiogenesis in goitrogenesis

Purpose of reviewThe thyroid is a highly vascular organ, and the thyroid vasculature is increased in goiter, induced either by thyrotropin (TSH) receptor stimulation or by tumorigenic transformation. This makes the thyroid an attractive model in which to study physiologic and pathologic angiogenesis and its regulation during organ growth. Recent findingsThyroid follicular cells secrete several angiogenic factors, eg, angiopoietins, vascular endothelial growth factors (VEGFs), fibroblast growth factors, and anti-angiogenic factors, eg, thrombospondin, angiostatin, and proteases, and their production is regulated by TSH through cyclic AMP or by other follicular cell growth factors. More surprisingly, thyroid follicular cells express the angiopoietin receptor, Tie-2 and possibly also the VEGF receptor, VEGFR1. The function of follicular cell Tie-2 expression remains a subject for conjecture, but recent work on angiopoietin structure and interactions with matrix proteins and on Tie-2 signaling has provided clues. Advances in defining endothelial and follicular cell biology also help understand the interdependence of angiogenesis and goitrogenesis. SummaryTo maintain euthyroidism, the thyroid must be able to respond rapidly to falling thyroid hormone levels with increased growth and function. Coordination of tissue remodeling within the thyroid is required for goiter formation. The mimicry of endothelial cells by thyroid cells may be related to the property of both cell types to form lumina. Limitation of goiter may be possible by inhibiting angiogenesis.