Evidence map›Paper›PMID 39073055›Full record

ArticleActa physiologica (Oxford, England)2024

Irisin preserves mitochondrial integrity and function in tubular epithelial cells after ischemia-reperfusion-induced acute kidney injury.

Yu Cui, Lu Yu, Wenqi Cong, Shan Jiang, Xingyu Qiu, Chunchun Wei, Gui Zheng, Jianhua Mao, Ruisheng Liu, Andreas Patzak and 4 more

Abstract read
In one paragraph

Article in Acta physiologica (Oxford, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Yu CuiKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lu YuKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Wenqi CongKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Shan JiangDepartment of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Xingyu QiuDepartment of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Chunchun WeiKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Gui ZhengKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jianhua MaoProvincial Key Laboratory of Neonatal Diseases, Department of Nephrology, National Clinical Research Center for Child Health, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-6076-3806
Ruisheng LiuDepartment of Molecular Pharmacology & Physiology, Hypertension and Kidney Research Center, Morsani College of Medicine, University of South Florida, Tampa, USA.
Andreas PatzakInstitute of Translational Physiology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID 0000-0002-1088-6875
Pontus B PerssonInstitute of Translational Physiology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Jianghua ChenKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-3282-3998
Liang ZhaoProvincial Key Laboratory of Neonatal Diseases, Department of Nephrology, National Clinical Research Center for Child Health, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0003-1846-5888
En Yin LaiKidney Disease Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0003-3074-6869

Funding

Tubuloglomerular feedback response in AKI to CKD transitionR01DK134028 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2022 to 2025
$2.6M
Role of tubuloglomerular feedback in the development of hypertension in diabetesR01HL142814 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2019 to 2022
$2.4M
Protection of donor kidney and transplanted graft function by modulating Na/K ATPase activityR01DK138092 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI WEI CHEN, RUISHENG LIU · 2024 to 2026
$2.0M
Treatment of lupus nephritis with nanoparticles that selectively target kidney glomeruliR01DK134000 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI RUISHENG LIU, Shyam S Mohapatra · 2023 to 2026
$1.9M
Tubuloglomerular feedback and salt-sensitive hypertensionR01DK098582 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2013 to 2016
$1.3M
NHLBI NIH HHS R01 HL142814NIDDK NIH HHS R01 DK098582NIDDK NIH HHS R01 DK134000NIDDK NIH HHS R01 DK134028NIDDK NIH HHS R01 DK138092The National Natural Science Foundation of China 81970647The National Natural Science Foundation of China 82100448The National Natural Science Foundation of China 82100796
6 · The paper itself

Abstract

aimsA myokine secreted by skeletal muscles during exercise called irisin mitigates ischemia-reperfusion (I/R) injury in epithelial cells of various organs by limiting damage to mitochondria. We test whether irisin may preserve the mitochondrial integrity and function in renal tubular epithelial cells and protect against ischemia-reperfusion-induced acute kidney injury (AKI).

methodsWe correlated serum irisin levels with serum creatinine and BUN levels from both AKI patients and healthy individuals. In mice with irisin administration, various renal injury markers such as serum creatinine, BUN, kidney injury molecule-1 (Kim-1), and neutrophil gelatinase-associated lipocalin (NGAL), and renal histopathology were assessed after I/R. To identify the potential mechanisms of the protective of irisin's protective effect, we perfused proximal tubules under confocal microscopy and analyzed kidney tissues by qPCR, western blot, and immunohistochemistry.

resultsSerum irisin correlated inversely with serum creatinine and BUN levels were significantly lower in AKI patients than in healthy subjects. Administering irisin to mice after I/R decreased biomarker levels for AKI including serum creatinine, BUN, Kim-1, NAGL and lessened histological changes. In kidney tissues of mice, irisin upregulated the mitochondrial autophagy marker protein microtubule-associated protein 1 light chain 3 (LC3), the mitochondrial autophagy pathway-related proteins PTEN-induced putative kinase 1 (PINK1) and Parkinson's disease 2 parkin (PARK2) and downregulated the reactive substrate protein sequestosome 1 (P62) and mitochondrial membrane proteins translocase of outer mitochondrial membrane 20 (TOM20) and translocase of inner mitochondrial membrane 23 (TIM23).

conclusionIrisin protects against renal I/R injury, which may involve the preservation of mitochondrial integrity and function.

Indexed as

Acute Kidney InjuryFibronectinsMice, Inbred C57BLMitochondriaReperfusion InjuryAnimalsEpithelial CellsFemaleHumansKidney TubulesMaleMiceFibronectinsFNDC5 protein, humanFNDC5 protein, mouseacute kidney injuryinflammasome activationirisinmitochondrial autophagyrenal ischemia–reperfusion

Identifiers

PMID39073055
PMCPMC11894518

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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.