The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity

Ren, Jianbing; Jiang, Jianlin; Ou, Weiming; Luo, Xiaodong; Xiang, Jianwen; Liu, Guosheng; Huang, Shui-qing; He, Longkai; Gan, Jiamin; Li, Hongping; Nie, Chuan

doi:10.3389/fped.2021.638432

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…The same research group later revealed that VEGF-induced STAT3 activation blocked retinal angiogenesis by downregulating local expression of erythropoietin (EPO) in Müller cells during phase 1 of OIR [106]. Ren et al's investigation in a rodent model exposed to hyperoxia demonstrated that hyperoxia-induced STAT3 signaling enhances hepcidin expression-a key protein involved in iron balance-suggesting a potential compensatory mechanism to counteract iron overload linked to neoangiogenesis and proposing targeting molecules to regulate iron regulation [107].…”

Section: The Central Role Of Nitro-oxidative Stress and Inflammatory ...mentioning

confidence: 99%

“…They emphasized its crucial function in negatively controlling JAK2/STAT3/VEGF-related angiogenesis, highlighting that its upregulation suppresses neoangiogenesis in the retinas of OIR mice [181]. Ren and colleagues, in a rodent model of ROP, demonstrated that S3I-201, a STAT3 pathway inhibitor, downregulated the expression of STAT3 and VEGF mRNA levels, effectively countering neoangiogenesis in ROP [107]. In another investigation, the E3 ubiquitin ligase synoviolin (SYVN1) was examined for its potential in ROP management.…”

Section: Targeting the Stat3 Signaling Pathway In Rop Managementmentioning

confidence: 99%

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Retinopathy of Prematurity—Targeting Hypoxic and Redox Signaling Pathways

Zhang,

Buonfiglio,

Fieß

et al. 2024

Antioxidants

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Retinopathy of prematurity (ROP) is a proliferative vascular ailment affecting the retina. It is the main risk factor for visual impairment and blindness in infants and young children worldwide. If left undiagnosed and untreated, it can progress to retinal detachment and severe visual impairment. Geographical variations in ROP epidemiology have emerged over recent decades, attributable to differing levels of care provided to preterm infants across countries and regions. Our understanding of the causes of ROP, screening, diagnosis, treatment, and associated risk factors continues to advance. This review article aims to present the pathophysiological mechanisms of ROP, including its treatment. Specifically, it delves into the latest cutting-edge treatment approaches targeting hypoxia and redox signaling pathways for this condition.

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Section: The Central Role Of Nitro-oxidative Stress and Inflammatory ...mentioning

confidence: 99%

Section: Targeting the Stat3 Signaling Pathway In Rop Managementmentioning

confidence: 99%

Retinopathy of Prematurity—Targeting Hypoxic and Redox Signaling Pathways

Zhang,

Buonfiglio,

Fieß

et al. 2024

Antioxidants

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“…Likewise, deletion of STAT3 increased lung injury and alveolar capillary leak in mice exposed to hyperoxia (Hokuto et al 2004 ). However, STAT3 activation in hyperoxic rats has also been linked to the pathogenesis of retinopathy of prematurity (Byfield et al 2009 ; Ren et al 2021 ).…”

Section: Hyperoxia Directly and Indirectly Modulates Diverse Signalin...mentioning

confidence: 99%

Oxygen toxicity: cellular mechanisms in normobaric hyperoxia

et al. 2022

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In clinical settings, oxygen therapy is administered to preterm neonates and to adults with acute and chronic conditions such as COVID-19, pulmonary fibrosis, sepsis, cardiac arrest, carbon monoxide poisoning, and acute heart failure. In non-clinical settings, divers and astronauts may also receive supplemental oxygen. In addition, under current standard cell culture practices, cells are maintained in atmospheric oxygen, which is several times higher than what most cells experience in vivo. In all the above scenarios, the elevated oxygen levels (hyperoxia) can lead to increased production of reactive oxygen species from mitochondria, NADPH oxidases, and other sources. This can cause cell dysfunction or death. Acute hyperoxia injury impairs various cellular functions, manifesting ultimately as physiological deficits. Chronic hyperoxia, particularly in the neonate, can disrupt development, leading to permanent deficiencies. In this review, we discuss the cellular activities and pathways affected by hyperoxia, as well as strategies that have been developed to ameliorate injury. Graphical abstract • Hyperoxia promotes overproduction of reactive oxygen species (ROS). • Hyperoxia dysregulates a variety of signaling pathways, such as the Nrf2, NF-κB and MAPK pathways. • Hyperoxia causes cell death by multiple pathways. • Antioxidants, particularly, mitochondria-targeted antioxidants, have shown promising results as therapeutic agents against oxygen toxicity in animal models.

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