ArticleInternational journal of clinical and experimental pathology2018
Clusterin (apolipoprotein J) facilitates NF-κB and Bax degradation and prevents I/R injury in heart transplantation.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Cardioprotective effects of the extracellular chaperone clusterin in acute myocardial infarction.European journal of clinical investigation · 2025Article
- A possible important regulatory role of estrogen in obstructive sleep apnea hypoventilation syndrome.Frontiers in medicine · 2025Review
- Lipoxin A4 improves myocardial ischemia/reperfusion injury through the Notch1-Nrf2 signaling pathway.Open life sciences · 2025Article
- Beneficial role of oleuropein in sepsis-induced myocardial injury. Possible Involvement of GSK-3β/NF-kB pathway.Acta cirurgica brasileira · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimIschemia-reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation and is a key factor in graft failure and long-term survival rate of recipients. Therefore, there is an urgent need for the development of new therapies to prevent I/R injury. Clusterin is a hetero-dimeric glycoprotein with an antiapoptotic function. In this study, we investigated whether clusterin was cardioprotective in heart transplantation against I/R injury using an
methodsHeart grafts from wild-type C57BL/6 mice were preserved in UW solution (control) or UW solution containing recombinant human apolipoprotein J (hr clusterin) for 24 hours. The preserved hearts were implanted into recipient mice of the same strain as the donors for 72 hours. The heart grafts were then taken for histopathological and gene expression analyses. An
resultsCold I/R caused severe morphologic myocardial injury to heart grafts from wild-type C57BL/6 mice whereas grafts from hr clusterin preservation showed less damage, as demonstrated by decreased cell apoptosis/death, decreased neutrophil infiltration, and the preservation of the normal structure of the heart. Clusterin reduced expression of p65, pre-inflammatory IL-1β, TNF-α, and the pro-apoptotic gene Bax while it enhanced expression of the anti-apoptotic gene Bcl-xL
conclusionClusterin is a promising target for preventing cold I/R injury in heart transplantation. This study also shows that the resultant protective effects of clusterin are mediated by NF-κB signaling and Bax/Bcl-xL expression.
Indexed as
Identifiers
31938213PMC6958155W3027063079What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.