Tomita Yohei, Usui-Ouchi Ayumi, Nilsson Anders K, Yang Jay, Ko Minji, Hellström Ann, Fu Zhongjie
Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Department of Ophthalmology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan.
Life (Basel). 2021 Oct 21;11(11):1119. doi: 10.3390/life11111119.
Retinopathy of prematurity is defined as retinal abnormalities that occur during development as a consequence of disturbed oxygen conditions and nutrient supply after preterm birth. Both neuronal maturation and retinal vascularization are impaired, leading to the compensatory but uncontrolled retinal neovessel growth. Current therapeutic interventions target the hypoxia-induced neovessels but negatively impact retinal neurons and normal vessels. Emerging evidence suggests that metabolic disturbance is a significant and underexplored risk factor in the disease pathogenesis. Hyperglycemia and dyslipidemia correlate with the retinal neurovascular dysfunction in infants born prematurely. Nutritional and hormonal supplementation relieve metabolic stress and improve retinal maturation. Here we focus on the mechanisms through which metabolism is involved in preterm-birth-related retinal disorder from clinical and experimental investigations. We will review and discuss potential therapeutic targets through the restoration of metabolic responses to prevent disease development and progression.
早产儿视网膜病变的定义为,早产出生后因氧环境和营养供应紊乱,在发育过程中出现的视网膜异常。神经元成熟和视网膜血管形成均受损,导致视网膜新血管进行代偿性但不受控的生长。目前的治疗干预针对缺氧诱导的新血管,但对视网膜神经元和正常血管有负面影响。新出现的证据表明,代谢紊乱是该疾病发病机制中一个重要但未得到充分研究的危险因素。高血糖和血脂异常与早产婴儿的视网膜神经血管功能障碍相关。营养和激素补充可缓解代谢应激并改善视网膜成熟。在此,我们通过临床和实验研究,重点关注代谢参与早产相关视网膜疾病的机制。我们将回顾并讨论通过恢复代谢反应来预防疾病发展和进展的潜在治疗靶点。