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

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dc.contributor.authorS K Sonn-
dc.contributor.authorE J Song-
dc.contributor.authorS Seo-
dc.contributor.authorY Y Kim-
dc.contributor.authorJ H Un-
dc.contributor.authorF J Yeo-
dc.contributor.authorD S Lee-
dc.contributor.authorS Jeon-
dc.contributor.authorMi Ni Lee-
dc.contributor.authorJ Jin-
dc.contributor.authorH Y Kweon-
dc.contributor.authorT K Kim-
dc.contributor.authorS Kim-
dc.contributor.authorS H Moon-
dc.contributor.authorS G Rhee-
dc.contributor.authorJ Chung-
dc.contributor.authorJ Yang-
dc.contributor.authorJ Han-
dc.contributor.authorE Y Choi-
dc.contributor.authorS B Lee-
dc.contributor.authorJ Yun-
dc.contributor.authorG T Oh-
dc.date.accessioned2022-03-07T15:31:42Z-
dc.date.available2022-03-07T15:31:42Z-
dc.date.issued2022-
dc.identifier.issn2213-2317-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/25551-
dc.description.abstractMitochondrial quality control (MQC) consists of multiple processes: the prevention of mitochondrial oxidative damage, the elimination of damaged mitochondria via mitophagy and mitochondrial fusion and fission. Several studies proved that MQC impairment causes a plethora of pathological conditions including cardiovascular diseases. However, the precise molecular mechanism by which MQC reverses mitochondrial dysfunction, especially in the heart, is unclear. The mitochondria-specific peroxidase Peroxiredoxin 3 (Prdx3) plays a protective role against mitochondrial dysfunction by removing mitochondrial reactive oxygen species. Therefore, we investigated whether Prdx3-deficiency directly leads to heart failure via mitochondrial dysfunction. Fifty-two-week-old Prdx3-deficient mice exhibited cardiac hypertrophy and dysfunction with giant and damaged mitochondria. Mitophagy was markedly suppressed in the hearts of Prdx3-deficient mice compared to the findings in wild-type and Pink1-deficient mice despite the increased mitochondrial damage induced by Prdx3 deficiency. Under conditions inducing mitophagy, we identified that the damaged mitochondrial accumulation of PINK1 was completely inhibited by the ablation of Prdx3. We propose that Prdx3 interacts with the N-terminus of PINK1, thereby protecting PINK1 from proteolytic cleavage in damaged mitochondria undergoing mitophagy. Our results provide evidence of a direct association between MQC dysfunction and cardiac function. The dual function of Prdx3 in mitophagy regulation and mitochondrial oxidative stress elimination further clarifies the mechanism of MQC in vivo and thereby provides new insights into developing a therapeutic strategy for mitochondria-related cardiovascular diseases such as heart failure.-
dc.publisherElsevier-
dc.titlePeroxiredoxin 3 deficiency induces cardiac hypertrophy and dysfunction by impaired mitochondrial quality control-
dc.title.alternativePeroxiredoxin 3 deficiency induces cardiac hypertrophy and dysfunction by impaired mitochondrial quality control-
dc.typeArticle-
dc.citation.titleRedox Biology-
dc.citation.number0-
dc.citation.endPage102275-
dc.citation.startPage102275-
dc.citation.volume51-
dc.contributor.affiliatedAuthorMi Ni Lee-
dc.contributor.alternativeName손성근-
dc.contributor.alternativeName송은주-
dc.contributor.alternativeName서승운-
dc.contributor.alternativeName김영연-
dc.contributor.alternativeName엄지현-
dc.contributor.alternativeName예준엽-
dc.contributor.alternativeName이다슬-
dc.contributor.alternativeName전세진-
dc.contributor.alternativeName이미니-
dc.contributor.alternativeNameJin-
dc.contributor.alternativeName권해연-
dc.contributor.alternativeName김태경-
dc.contributor.alternativeName김신애-
dc.contributor.alternativeName문신혜-
dc.contributor.alternativeName이서구-
dc.contributor.alternativeName정종경-
dc.contributor.alternativeName양재문-
dc.contributor.alternativeName한진-
dc.contributor.alternativeName최의영-
dc.contributor.alternativeName이성배-
dc.contributor.alternativeName윤진호-
dc.contributor.alternativeName오구택-
dc.identifier.bibliographicCitationRedox Biology, vol. 51, pp. 102275-102275-
dc.identifier.doi10.1016/j.redox.2022.102275-
dc.subject.keywordPeroxiredoxin 3-
dc.subject.keywordHeart failure-
dc.subject.keywordMitochondrial quality control-
dc.subject.keywordDamaged mitochondria-
dc.subject.keywordMitophagy-
dc.subject.keywordPINK1-
dc.subject.localPeroxiredoxin 3-
dc.subject.localHeart failure-
dc.subject.localheart failure-
dc.subject.localHeart Failure-
dc.subject.localMitochondrial quality control-
dc.subject.localDamaged mitochondria-
dc.subject.localmitophagy-
dc.subject.localMitophagy-
dc.subject.localPINK1-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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