Peroxiredoxin 3 deficiency induces cardiac hypertrophy and dysfunction by impaired mitochondrial quality control

Sonn, Seong Keun; Song, Eun Ju; Seo, Seungwoon; Kim, Young Yeon; Um, Jee-Hyun; Yeo, Franklin Joonyeop; Lee, Da Seul; Jeon, Sejin; Lee, Mi-Ni; Jin, Jing; Kweon, Hyae Yon; Kim, Tae Kyeong; Kim, Sinai; Moon, Shin Hye; Rhee, Sue Goo; Chung, Jongkyeong; Yang, Jaemoon; Han, Jing; Choi, Eui‐Young; Lee, Sung Bae; Yun, Jeanho; Oh, Goo Taeg

doi:10.1016/j.redox.2022.102275

Cited by 21 publications

(15 citation statements)

References 36 publications

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“…Zhang et al constructed a secondary oocyte OS injury model and found that the ATP level and mitochondrial membrane potential were both decreased; this was accompanied by spindle damage [ 54 ]. Recombinant peroxiredoxin 3 (Prdx3) is localized in the mitochondria and acts as a key regulator of mitochondrial ROS [ 55 ]. Global gene expression analysis of aged mouse oocytes revealed reduced Prdx3 mRNA expression and increased sensitivity of oocytes to OS [ 56 ].…”

Section: Pathological Mechanisms Related With Os In Ovarian Agingmentioning

confidence: 99%

The role of oxidative stress in ovarian aging: a review

et al. 2022

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Ovarian aging refers to the process by which ovarian function declines until eventual failure. The pathogenesis of ovarian aging is complex and diverse; oxidative stress (OS) is considered to be a key factor. This review focuses on the fact that OS status accelerates the ovarian aging process by promoting apoptosis, inflammation, mitochondrial damage, telomere shortening and biomacromolecular damage. Current evidence suggests that aging, smoking, high-sugar diets, pressure, superovulation, chemotherapeutic agents and industrial pollutants can be factors that accelerate ovarian aging by exacerbating OS status. In addition, we review the role of nuclear factor E2-related factor 2 (Nrf2), Sirtuin (Sirt), mitogen-activated protein kinase (MAPK), protein kinase B (AKT), Forkhead box O (FoxO) and Klotho signaling pathways during the process of ovarian aging. We also explore the role of antioxidant therapies such as melatonin, vitamins, stem cell therapies, antioxidant monomers and Traditional Chinese Medicine (TCM), and investigate the roles of these supplements with respect to the reduction of OS and the improvement of ovarian function. This review provides a rationale for antioxidant therapy to improve ovarian aging.

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Section: Pathological Mechanisms Related With Os In Ovarian Agingmentioning

confidence: 99%

The role of oxidative stress in ovarian aging: a review

et al. 2022

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“…For instance, KH176, a chemical derivative of a water-soluble form of vitamin E, enhanced mitophagy in neurons from subjects with or without Parkin mutation, suggesting its pro-mitophagy effect in a Parkin-independent manner 173 . KH176 exerts its anti-oxidative effects through direct interaction with peroxiredoxins 174 , while peroxiredoxin 3 175 and peroxiredoxin 6 176 have been found to be involved in mitophagy. Another study showed that mitochondria-targeted antioxidant, MitoQ rescued mitophagy, mitochondrial dysfunction and apoptosis through Nrf2 and PINK1 rather than its direct antioxidative effect 177 .…”

Section: The Bridges Between Ros and Mitophagymentioning

confidence: 99%

Mitophagy and reactive oxygen species interplay in Parkinson’s disease

Xiao

Kuruvilla

Tan

2022

npj Parkinsons Dis.

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Mitophagy impairment and oxidative stress are cardinal pathological hallmarks in Parkinson’s disease (PD), a common age-related neurodegenerative condition. The specific interactions between mitophagy and reactive oxygen species (ROS) have attracted considerable attention even though their exact interplay in PD has not been fully elucidated. We highlight the interactions between ROS and mitophagy, with a focus on the signalling pathways downstream to ROS that triggers mitophagy and draw attention to potential therapeutic compounds that target these pathways in both experimental and clinical models. Identifying a combination of ROS inhibitors and mitophagy activators to provide a physiologic balance in this complex signalling pathways may lead to a more optimal outcome. Deciphering the exact temporal relationship between mitophagy and oxidative stress and their triggers early in the course of neurodegeneration can unravel mechanistic clues that potentially lead to the development of compounds for clinical drug trials focusing on prodromic PD or at-risk individuals.

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“…Our results showed that mice with PRDX3 knockdown were more susceptible to UUO-induced renal fibrosis, but whether the same phenomenon occurs in mice with deletion of PRDX3 gene remains unclear. Previous study found that PRDX3 knockout aggravated myocardial fibrosis and ventricular remodeling after myocardial infarction in mice [ 34 ]. Based on this result, it was reasonable to believe that mice with PRDX3 knocked out may be more vulnerable to renal fibrosis when subjected to UUO.…”

Section: Discussionmentioning

confidence: 99%

The E3 ubiquitin ligase TRIM39 modulates renal fibrosis induced by unilateral ureteral obstruction through regulating proteasomal degradation of PRDX3

Jian,

Liu,

Zheng

et al. 2024

Cell Death Discov.

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Renal fibrosis is considered to be the ultimate pathway for various chronic kidney disease, with a complex etiology and great therapeutic challenges. Tripartite motif-containing (TRIM) family proteins have been shown to be involved in fibrotic diseases, but whether TRIM39 plays a role in renal fibrosis remain unexplored. In this study, we investigated the role of TRIM39 in renal fibrosis and its molecular mechanism. TRIM39 expression was analyzed in patients’ specimens, HK-2 cells and unilateral ureteral obstruction (UUO) mice were used for functional and mechanistic studies. We found an upregulated expression of TRIM39 in renal fibrosis human specimens and models. In addition, TRIM39 knockdown was found efficient for alleviating renal fibrosis in both UUO mice and HK-2 cells. Mechanistically, we demonstrated that TRIM39 interacted with PRDX3 directly and induced ubiquitination degradation of PRDX3 at K73 and K149 through the K48 chain, which resulted in ROS accumulation and increased inflammatory cytokine generation, and further aggravated renal fibrosis. It provided an emerging potential target for the therapies of renal fibrosis.

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Peroxiredoxin 3 deficiency induces cardiac hypertrophy and dysfunction by impaired mitochondrial quality control

Cited by 21 publications

References 36 publications

The role of oxidative stress in ovarian aging: a review

The role of oxidative stress in ovarian aging: a review

Mitophagy and reactive oxygen species interplay in Parkinson’s disease

The E3 ubiquitin ligase TRIM39 modulates renal fibrosis induced by unilateral ureteral obstruction through regulating proteasomal degradation of PRDX3

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