Evidence map›Paper›PMID 40045562›Full record

ArticleChinese medical journal2026

LncRNA H19 overexpression protects against acute kidney injury after cardiopulmonary bypass via activating Pink1/Parkin-mediated mitophagy.

Mingru Zhang, Min Liu, Tianlong Wang, Yingjie Du, Yimeng Chen, Yafan Bai, Yue Zhang, Dinghao Xue, Bingyang Ji, Guyan Wang

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In one paragraph

Article in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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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

5 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

10 authors.

Mingru ZhangDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Min LiuDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Tianlong WangDepartment of Cardiopulmonary Bypass, Fuwai Hospital, National Center for Cardiovascular Disease, State Key Laboratory of Cardiovascular Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100037, China.
Yingjie DuDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Yimeng ChenDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Yafan BaiDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Yue ZhangDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Dinghao XueDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Bingyang JiDepartment of Cardiopulmonary Bypass, Fuwai Hospital, National Center for Cardiovascular Disease, State Key Laboratory of Cardiovascular Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100037, China.
Guyan WangDepartment of Anesthesiology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiopulmonary bypass-associated acute kidney injury (CPB-AKI) is a serious and common complication following cardiopulmonary bypass (CPB), leading to worse outcomes and higher mortality. However, the underlying pathological mechanisms of CPB-AKI remain largely unknown. This study aimed to investigate the role of long non-coding RNA H19 ( H19 ) in regulating CPB-AKI.

methodsWe examined the expressions of H19 and mitophagy-related proteins in a CPB-AKI rat model and HK-2 cells following oxygen-glucose deprivation/reperfusion (OGD/R). In vivo , lentiviral-mediated overexpression of H19 was induced in the kidney through tail vein injection. We then evaluated renal functions, kidney pathological damage, levels of inflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and IL-10), neutrophil infiltration, and the activation of PTEN-induced putative kinase 1 (Pink1)/Parkin-mediated mitophagy following CPB-AKI. In vitro , small interfering RNA (siRNA) was used to downregulate H19 expression in HK-2 cells. We also examined cell viability, apoptosis, inflammation, and Pink1/Parkin-mediated mitophagy after OGD/R.

resultsWe demonstrated an increase in H19 expression and activation of Pink1/Parkin-mediated mitophagy in the rat model of CPB-AKI and HK-2 cells following OGD/R. In the rat models of CPB-AKI, lentivirus-mediated overexpression of H19 significantly attenuated renal injury, characterized by better renal function, reduced tissue damage, decreased neutrophil infiltration, and lower inflammatory cytokine release ( P  <0.05). Notably, overexpression of H19 significantly activated Pink1/Parkin-mediated mitophagy. Furthermore, in vitro , downregulation of H19 by specific siRNA in HK-2 cells significantly decreased cell viability, worsened HK-2 injury after OGD/R, increased inflammatory cytokine release, and decreased Pink1/Parkin-mediated mitophagy activity, promoting cell apoptosis ( P  <0.05).

conclusionsThese findings suggest that H19 overexpression may protect against CPB-AKI by activating Pink1/Parkin-mediated mitophagy and decreasing inflammatory responses and cellular apoptosis. Thus, H19 overexpression might be a promising therapeutic target for treating CPB-AKI.

Indexed as

Acute Kidney InjuryCardiopulmonary BypassMitophagyProtein KinasesRNA, Long NoncodingUbiquitin-Protein LigasesAnimalsApoptosisCell LineHumansMaleRatsRats, Sprague-DawleyH19 long non-coding RNAparkin proteinProtein KinasesRNA, Long NoncodingUbiquitin-Protein LigasesAcute kidney injuryCardiopulmonary bypassMitophagyParkin proteinPink1/ParkinPTEN-induced putative kinase

Identifiers

PMID40045562
PMCPMC12999110

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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.