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Last update 08 May 2025

PRDX6

Last update 08 May 2025

Basic Info

Synonyms

1-Cys, 1-Cys peroxiredoxin, 1-Cys PRX

+ [21]

Introduction

Thiol-specific peroxidase that catalyzes the reduction of hydrogen peroxide and organic hydroperoxides to water and alcohols, respectively (PubMed:10893423, PubMed:9497358). Can reduce H(2)O(2) and short chain organic, fatty acid, and phospholipid hydroperoxides (PubMed:10893423). Also has phospholipase activity, can therefore either reduce the oxidized sn-2 fatty acyl group of phospholipids (peroxidase activity) or hydrolyze the sn-2 ester bond of phospholipids (phospholipase activity) (PubMed:10893423, PubMed:26830860). These activities are dependent on binding to phospholipids at acidic pH and to oxidized phospholipds at cytosolic pH (PubMed:10893423). Plays a role in cell protection against oxidative stress by detoxifying peroxides and in phospholipid homeostasis (PubMed:10893423). Exhibits acyl-CoA-dependent lysophospholipid acyltransferase which mediates the conversion of lysophosphatidylcholine (1-acyl-sn-glycero-3-phosphocholine or LPC) into phosphatidylcholine (1,2-diacyl-sn-glycero-3-phosphocholine or PC) (PubMed:26830860). Shows a clear preference for LPC as the lysophospholipid and for palmitoyl CoA as the fatty acyl substrate (PubMed:26830860).

Drugs associated with PRDX6

Prezatide copper acetate

Target

PRDX6

Mechanism

PRDX6 modulators [+1]

Active Org.-

Originator Org.-

Active Indication

Burns [+2]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

United States

First Approval Date01 Jan 2011

PIP-2

Target

CYBB x PRDX6

Mechanism

CYBB inhibitors [+1]

Active Org.

Peroxitech Therapeutics, Inc.

Originator Org.

University of Pennsylvania

Active Indication

Acute Lung Injury

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN119403810

Patent Mining

Target

PRDX6

Mechanism-

Active Org.

VasThera Co., Ltd.

Originator Org.

VasThera Co., Ltd.

Active Indication

Cardiovascular Diseases [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with PRDX6

IRCT20170314033069N6

/ SuspendedPhase 3IIT

A comparative study between endotracheal tube and I-GEL in gynecological laparoscopic surgeries under general anesthesia; A double blind clinical trial study

Start Date23 Aug 2023

Sponsor / Collaborator-

CTRI/2023/07/055820

/ Not yet recruitingNot ApplicableIIT

Comparison of I-gel airway vs SLIPA 2G airway in paediatric paitents undergoing general anaesthesia with caudal epidural anaesthesia- one year randomised clinical trial - nil

Start Date13 Aug 2023

Sponsor / Collaborator-

CTRI/2023/08/055942

/ RecruitingPhase 4

Comparison of BrimacombeScore and first-attempt success rate of Ambu AuraGain and I-gel in anaesthetised adult patients: A Prospective open label study

Start Date01 Aug 2023

Sponsor / Collaborator

AIIMS Kalyani

100 Clinical Results associated with PRDX6

100 Translational Medicine associated with PRDX6

0 Patents (Medical) associated with PRDX6

1,015

Literatures (Medical) associated with PRDX6

31 Dec 2025·Experimental Lung Research

Involvement of PRDX6 in the protective role of MANF in acute lung injury in rats

Article

Author: Shen, Qiying ; Wang, Lixia ; Shen, Yujun ; Yang, Xiuli ; Xiao, Xueying ; Zhou, Leiying

Aim/Purpose of the study: Acute lung injury (ALI) is a severe respiratory disease with high mortality, mainly due to overactivated oxidative stress and subsequent pyroptosis. Mesencephalic astrocyte-derived neurotrophic factor (MANF), an inducible secretory endoplasmic reticulum (ER) stress protein, inhibits lipopolysaccharide (LPS)-induced acute lung injury (ALI). However, the exact molecular mechanism remains unclear. Peroxiredoxin 6 (PRDX6), a peroxidase with a dual enzymatic function, is essential in regulating oxidative stress, which is closely associated with ALI. Furthermore, PRDX6 is an interacting protein of MANF. Therefore, this study aims to investigate the role of PRDX6 in the protective effect of MANF on ALI.Materials and Methods: In this study, we used LPS to establish the LPS-induced ALI model. Recombinant human MANF was administrated to wide-type (WT) and PRDX6 knockout (PRDX6^-/-) rats.Results: In WT rats, MANF reversed the increases of PRDX6, ROS overgeneration, and pyroptosis-related protein-Gasdermin D (GSDMD) induced by LPS challenge. In PRDX6^-/- rats, ROS generation, the protein level of GSDMD-N, and lung injury were not significantly decreased after human recombinant MANF administration in LPS-induced ALI.Conclusions: PRDX6 is involved in the protective role of MANF on ALI. It is a key target molecule for MANF to exert ALI inhibitory effects.

01 Dec 2025·Human & Experimental Toxicology

KLF9 mediates NLRP3 inflammasome and reactive oxygen species to mediate pyroptosis in trophoblasts

Article

Author: Chen, Min ; Li, Qian

IntroductionThe objective of this study was to explore the effect of KLF9 on oxidative stress (OS) and NLRP3-mediated inflammation in preeclampsia (PE).Methods Lipopolysaccharide (LPS)+adenosine triphosphate (ATP)-induced HTR-8/SVneo cells were used as an in vitro PE inflammation cell model. shRNA was used to interfere with KLF9 expression (sh-KLF9) to assess the transfection efficiency and the effect of KLF9 on cell proliferation, migration, and invasion. ELISA was performed to detect OS-related factors and inflammatory cytokines. Reactive oxygen species (ROS) levels and pyroptosis were analyzed using DCFH-DA and TUNEL staining. LPS and ATP induced HTR-8/SVneo cells were co-transfected with sh-PRDX6/sh-KLF9 to explore the potential regulatory effect of KLF9 on PRDX6. Results LPS+ATP stimulation increased KLF9 expression in the PE cell model. Specifically, reducing KLF9 levels alleviated morphological damage and enhanced proliferation, migration, and invasion in the in vitro PE cell models. Moreover, inhibiting KLF9 expression decreased protein expression of NLRP3, GSDMD-N, cleaved caspase-1, and cleaved-IL-1β, suppressing cell death in LPS+ATP-induced HTR-8/SVneo cells. Analysis of OS indicators revealed that downregulating KLF9 expression restrained intracellular ROS production, decreased MDA expression, and increased SOD and CAT levels. KLF9 regulated the transcription of PRDX6 to attenuate OS and pyroptosis. Knockdown of PRDX6 partially abolished the effect of KLF9 downregulation on OS and pyroptosis of LPS+ATP-induced HTR-8/SVneo cells, as evidenced by the inhibition of cell proliferation, migration, and invasion, as well as the enhanced activity of the NLRP3 inflammasome. ConclusionDownregulation of KLF9 enhances trophoblast cell invasion and reduces OS and NLRP3 inflammasome activation-mediated pyroptosis.

01 Dec 2025·Immunologic Research

α-Amanitin aggravates hepatic injury by activating oxidative stress and mitophagy via peroxiredoxin 6 inhibition

Article

Author: Duan, Hongdan ; Duan, Xueqiong ; Ye, Yong ; Fu, Yangshan ; Cheng, Kerun ; Cheng, Zhongfeng ; Tang, Yan

Mushroom poisoning is mainly caused by α-amanitin (α-AMA), and there is currently no effective drug to treat α-AMA poisoning. Therefore, it is particularly important to find early diagnostic markers for α-AMA injury. Hepatic injury models induced by α-AMA were established both in hepatic cells and mice. The cell viability of human normal hepatic cells after α-AMA treatment was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Liver function parameters was assessed by the Enzyme-Linked Immunosorbent Assay (ELISA). Furthermore, oxidative stress was detected by 2',7'-Dichlorofluorescin Diacetate (DCFH-DA) and Dihydroethidium (DHE) staining. Autophagy- and apoptosis-related proteins were assessed by Western blot and immunofluorescence staining. We applied Hematoxylin and Eosin (H&E), Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and Oil Red O (ORO) staining to observe the degree of cell damage and hepatocyte apoptosis. In addition, mitochondrial membrane potential was also determined by JC-1 immunofluorescence staining and flow cytometry. The results showed that α-AMA decreased cell viability in a dose-dependent manner. In addition, the levels of alanine aminotransferase (ALT), aspartate transaminase (AST) and mitochondrial reactive oxygen species (mtROS) were observed to increase in the α-AMA-treated groups, whereas antioxidants superoxide dismutase (SOD) levels were reduced. Moreover, α-AMA promoted hepatocyte mitophagy and apoptosis, which were alleviated by PRDX6 overexpression. Finally, PRDX6 and Parkin were found to accumulate in mitochondria and α-AMA activated mitophagy by silencing PRDX6. Collectively, our results demonstrated that α-AMA activates oxidative stress and mitophagy by inhibiting the expression of PRDX6, leading to hepatic injury. These findings from both in vitro and in vivo models provide insights into the toxicological mechanisms of α-AMA, underscoring the potential of PRDX6 as a therapeutic target for treating α-AMA-induced hepatotoxicity. HIGHLIGHTS: α-AMA leads to ROS accumulation and activates oxidative stress. α-AMA promotes hepatocyte mitophagy and apoptosis. PRDX6 alleviates α-AMA-induced hepatic injury. PRDX6 mediates mitophagy through Parkin.

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PRDX6

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