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  3. Acetylation of PRDX5 aggravates the oxidative stress and apoptosis of retinal neurons induced by ischemia-reperfusion

Acetylation of PRDX5 aggravates the oxidative stress and apoptosis of retinal neurons induced by ischemia-reperfusion

  • Tissue Cell. 2026 Aug:101:103408. doi: 10.1016/j.tice.2026.103408.
Shuang Lu 1,  Lewen Wang 2,  Keting Wang 3,  Kun Xiong 4,  Weitao Yan 5,  Chi Zhang 6
Affiliations

Affiliations

  • 1 Department of Neurosurgery, The Institute of Skull Base Surgery and Neurooncology at Hunan Province, Xiangya Hospital, Central South University, Changsha 410008 China; Department of Anatomy and Neurobiology, School of Xiangya Basic Medical Science, Central South University, Changsha, Hunan 410013, China. Electronic address: [email protected].
  • 2 Department of Anatomy and Neurobiology, School of Xiangya Basic Medical Science, Central South University, Changsha, Hunan 410013, China. Electronic address: [email protected].
  • 3 Department of Anatomy and Neurobiology, School of Xiangya Basic Medical Science, Central South University, Changsha, Hunan 410013, China. Electronic address: [email protected].
  • 4 Department of Anatomy and Neurobiology, School of Xiangya Basic Medical Science, Central South University, Changsha, Hunan 410013, China. Electronic address: [email protected].
  • 5 Department of Anatomy and Neurobiology, School of Xiangya Basic Medical Science, Central South University, Changsha, Hunan 410013, China; The Key Laboratory of Brain Science Research & Transformation In Tropical Environment Of Hainan Province, Hainan Medical University, Haikou, Hainan 571199, China. Electronic address: [email protected].
  • 6 Department of Neurosurgery, The Institute of Skull Base Surgery and Neurooncology at Hunan Province, Xiangya Hospital, Central South University, Changsha 410008 China. Electronic address: [email protected].
PMID: 41740330 DOI: 10.1016/j.tice.2026.103408
Abstract

Retinal ischemia-reperfusion (I/R) injury is an important pathological mechanism of glaucoma. The role of peroxiredoxin 5 (PRDX5) in this process remains unclear. An acute high intraocular pressure (aHIOP) mouse model was used, and oxygen and glucose deprivation and reoxygenation (OGD/R) injury in R28 cells was used to investigate the role of PRDX5 in retinal I/R injury. The role of PRDX5 was assessed by hematoxylin-eosin (HE) staining, TUNEL staining, and Western blotting (WB) in vivo. Cell viability, Lactate Dehydrogenase (LDH) release, propidium iodide (PI) staining, Reactive Oxygen Species (ROS), mitochondrial membrane potential assay, and WB analyses were conducted to validate the effect of PRDX5 in vitro. The effects of PRDX5 acetylation were analyzed using nicotinamide and nicotinamide riboside chloride (NRC) in the OGD/R model. Knocking down PRDX5 expression exacerbated OGD/R-induced Apoptosis and oxidative stress. Overexpressing PRDX5 reduced OGD/R-induced Apoptosis and oxidative stress. Overexpressing PRDX5 significantly attenuated retinal tissue damage and neuronal Apoptosis after I/R in vivo. OGD/R increased PRDX5 acetylation in R28 cells. NAM treatment increased PRDX5 acetylation induced by OGD/R, concomitant with increased ROS levels and Apoptosis in R28 cells. NRC treatment reduced OGD/R-induced PRDX5 acetylation, concomitantly decreasing ROS production and attenuating Apoptosis. Notably, inhibiting deacetylation abolished the protective effect of PRDX5 overexpression. Our study suggested that PRDX5 plays a vital role in protecting against oxidative stress and Apoptosis in retinal I/R injury. The acetylation of PRDX5 inhibits its antioxidant and anti-apoptotic functions.

Keywords

Acetylation; Apoptosis; Ischemia-reperfusion; PRDX5; Retinal neuron.

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