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Although glutamine metabolism plays a crucial role in macrophage polarization, its regulatory effect on macrophages involved in chemical burn\u2010induced corneal injury is not known. Here, we elucidated the connection between the reprogramming of glutamine metabolism in macrophages and the development of alkali burn\u2010induced CoNV. Glutaminase 1 (GLS1) expression was upregulated in the mouse corneas damaged with alkali burns and was primarily located in F4\/80\u2010positive macrophages. Treatment with a selective oral GLS1 inhibitor, CB\u2010839 (telaglenastat), significantly decreased the distribution of polarized M2 macrophages in the alkali\u2010injured corneas and suppressed the development of CoNV. In vitro studies further demonstrated that glutamine deprivation or CB\u2010839 treatment inhibited the proliferation, adhesion, and M2 polarization of bone marrow\u2010derived macrophages (BMDMs) from C57BL\/6J mice. CB\u2010839 treatment markedly attenuated the secretion of proangiogenic factors, including vascular endothelial growth factor\u2010A (VEGF\u2010A) and platelet\u2010derived growth factor\u2010BB (PDGF\u2010BB) from interleukin\u20104\u2010 (IL\u20104\u2010) regulated M2 macrophages. Our findings revealed that GLS1 inhibition or glutamine deprivation prevented alkali\u2010induced CoNV by inhibiting the infiltration and M2 polarization of macrophages. This work suggests that pharmacological GLS1 inhibition is a feasible and effective treatment strategy for chemical burn\u2010related CoNV in humans.<\/jats:p>","DOI":"10.1155\/2022\/1106313","type":"journal-article","created":{"date-parts":[[2022,3,19]],"date-time":"2022-03-19T20:05:09Z","timestamp":1647720309000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Pharmacological Inhibition of Glutaminase 1 Attenuates Alkali\u2010Induced Corneal Neovascularization by Modulating 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