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Despite current therapies, ROP continues to be a highly debilitating disease. Our advancing knowledge of the pathogenesis of ROP has encouraged investigations into new antivasculogenic therapies. The purpose of this article is to review the findings on the pathophysiological mechanisms that contribute to the transition between the first and second phases of ROP and to investigate new potential therapies. Oxygen has been well characterized for the key role that it plays in retinal neoangiogenesis. Low or high levels of pO\n                    <jats:sub>2<\/jats:sub>\n                    regulate the normal or abnormal production of hypoxia\u2010inducible factor 1 and vascular endothelial growth factors (VEGF), which are the predominant regulators of retinal angiogenesis. Although low oxygen saturation appears to reduce the risk of severe ROP when carefully controlled within the first few weeks of life, the optimal level of saturation still remains uncertain. IGF\u20101 and Epo are fundamentally required during both phases of ROP, as alterations in their protein levels can modulate disease progression. Therefore, rhIGF\u20101 and rhEpo were tested for their abilities to prevent the loss of vasculature during the first phase of ROP, whereas anti\u2010VEGF drugs were tested during the second phase. At present, previous hypotheses concerning ROP should be amended with new pathogenetic theories. Studies on the role of genetic components, nitric oxide, adenosine, apelin and \u03b2\u2010adrenergic receptor have revealed new possibilities for the treatment of ROP. The genetic hypothesis that single\u2010nucleotide polymorphisms within the \u03b2\u2010ARs play an active role in the pathogenesis of ROP suggests the concept of disease prevention using \u03b2\u2010blockers. In conclusion, all factors that can mediate the progression from the avascular to the proliferative phase might have significant implications for the further understanding and treatment of ROP.\n                  <\/jats:p>","DOI":"10.1111\/aos.12049","type":"journal-article","created":{"date-parts":[[2013,4,26]],"date-time":"2013-04-26T00:46:49Z","timestamp":1366937209000},"page":"2-20","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":159,"title":["The pathophysiology of retinopathy of prematurity: an update of previous and recent 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