Protective effects of PARP1-inhibitory compound in dry age-related macular degeneration

Ho, Jeongmin; Jang, Ki-Hong; Koo, Tae‐Sung; Park, Changmin; Kim, Young-Hoon; Kim, Eun‐Hee

doi:10.1016/j.biopha.2020.111041

Cited by 7 publications

(4 citation statements)

References 39 publications

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“…PARP-1, an NAD+-consuming enzyme, competes with SIRT1 for the same NAD+ pool. Increased PARP-1 activity leads to SIRT1 inhibition, making PARP-1 inhibitors protective against aging vessels [153,164].…”

Section: Sirt Activators Telomerase Enhancers and Senolyticsmentioning

confidence: 99%

Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress

Cui,

Buonfiglio,

Pfeiffer

et al. 2024

Biomedicines

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Acknowledged as a significant pathogenetic driver for numerous diseases, aging has become a focal point in addressing the profound changes associated with increasing human life expectancy, posing a critical concern for global public health. Emerging evidence suggests that factors influencing vascular aging extend their impact to choroidal and retinal blood vessels. The objective of this work is to provide a comprehensive overview of the impact of vascular aging on ocular blood vessels and related diseases. Additionally, this study aims to illuminate molecular insights contributing to vascular cell aging, with a particular emphasis on the choroid and retina. Moreover, innovative molecular targets operating within the domain of ocular vascular aging are presented and discussed.

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Section: Sirt Activators Telomerase Enhancers and Senolyticsmentioning

confidence: 99%

Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress

Cui,

Buonfiglio,

Pfeiffer

et al. 2024

Biomedicines

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“…PARP (poly-ADP-ribose polymerase) inhibitors, such as olaparib, rucaparib, and niraparib, have been recently added to the prostate cancer therapy armamentarium since they were shown to prolong overall survival in patients with metastatic castration-resistant prostate cancer (mCRPC) [ 106 ] (Table 1 ). PARP1-dependent cell death in the retinal pigment epithelium has also been implicated in age-related macular degeneration (AMD), while studies have shown that PARP inhibitors might exert a protective role in dry AMD [ 107 ]. PARP inhibitors might also be beneficial in the treatment of photoreceptor degeneration in hereditary retinal dystrophies or glaucoma [ 108 , 109 ].…”

Section: Reviewmentioning

confidence: 99%

Potential Ophthalmological Side Effects Induced by Anti-Neoplastic Regimens for the Treatment of Genitourinary Cancers: A Review

Sakellakis¹,

Spathas²,

Tsaousis³

et al. 2022

Cureus

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The outcomes of patients with genitourinary (GU) cancers have been steadily improving in recent years. Novel therapies have entered our armamentarium, while several other regimens are currently being studied in clinical trials. This recent explosion of new agents has improved patient survival and the quality of life for patients, but has also significantly increased the frequency of several side effects. The current review will focus on the potential ocular adverse reactions of GU neoplastic treatments. The broad spectrum of manifestations of ocular toxicity underscores the uniqueness and complexity of the anatomic, physiologic, and metabolic features of the human eye. Most side effects are mild in severity and transient, but some can be severe, disabling, and irreversible. Clinicians should be aware of complications that might be vision threatening and impact the patient's quality of life. In this review, we focused on the ocular toxicity of the antineoplastic regimens that are currently used for the treatment of GU, including prostate cancer, bladder cancer, renal cell carcinoma, testicular cancer, pheochromocytoma, adrenocortical carcinoma, and penile cancer.

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“…HiPSC-derived RPE from AMD patients can be used to model the early pathogenesis of AMD [ 33 ]. Sodium iodate (NaIO 3 ), an oxidizing agent, has been extensively employed to replicate human AMD in animal models and caused thinner retinas as demonstrated by optical coherence tomography (OCT) and decreased amplitudes of the a- and b-waves as confirmed by electroretinogram (ERG) [ 34 , 35 ]. A blue light exposure-induced animal AMD model showed the degeneration of the retinal layer as determined by fundus imaging [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA NORAD defects deteriorate the formation of age-related macular degeneration

Zhang

Jiang

Zhou

et al. 2023

Aging

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Long noncoding RNAs (lncRNAs) play important roles in the development of age-related macular degeneration (AMD). However, the effect of long non-coding RNA activated by DNA damage (NORAD) on AMD remains unknown. This study aimed to investigate the effect of NORAD on RPE cell senescence and degeneration. Irradiated adult retinal pigment epithelial cell line-19 (ARPE-19) and sodium iodate-treated mice were used as in vitro and in vivo AMD models. Results showed that irradiation-induced AMD characteristics of ARPE-19 and NORAD-knockdown aggravated cell cycle arrest in the G2/M phase, cell apoptosis and cell senescence along with the increased expression of phosphorylated P53 (p-P53) and P21. AMD factors C3, ICAM-1, APP, APOE, and VEGF-A were also increased by NORAD-knockdown. Moreover, NORAD-knockdown increased irradiation-induced reduction of mitochondrial homeostasis factors, (i.e., TFAM and POLG) and mitochondrial respiratory chain complex genes (i.e., ND1 and ND5) along with mitochondrial reactive oxygen species (ROS). We also identified a strong interaction of NORAD and PGC-1α and sirtuin 1 (SIRT1) in ARPE-19; that is, NORAD knockdown increases the acetylation of PGC-1α. In NORAD knockout mice, NORAD-knockout accelerated the sodium iodate-reduced retinal thickness reduction, function impairment and loss of retinal pigment in the fundus. Therefore, NORAD-knockdown accelerates retinal cell senescence, apoptosis, and AMD markers via PGC-1α acetylation, mitochondrial ROS, and the p-P53–P21signaling pathway, in which NORAD-mediated effect on PGC-1α acetylation might occur through the direct interaction with PGC-1α and SIRT1.

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Protective effects of PARP1-inhibitory compound in dry age-related macular degeneration

Cited by 7 publications

References 39 publications

Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress

Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress

Potential Ophthalmological Side Effects Induced by Anti-Neoplastic Regimens for the Treatment of Genitourinary Cancers: A Review

LncRNA NORAD defects deteriorate the formation of age-related macular degeneration

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