Evidence map›Paper›PMID 34000358›Full record

ArticleInternational journal of cardiology2021

Abnormal apelin-ACE2 and SGLT2 signaling contribute to adverse cardiorenal injury in patients with COVID-19.

Xue-Ting Li, Mi-Wen Zhang, Zhen-Zhou Zhang, Yu-Dan Cao, Xiao-Yan Liu, Ran Miao, Yuan Xu, Xiao-Fang Song, Jia-Wei Song, Ying Liu and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 10% of its field
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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  13. SGLT2 Inhibitors in Long COVID Syndrome: Is There a Potential Role?Journal of cardiovascular development and disease · 2023
    Review
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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 at 2 institutions in 1 country.

Xue-Ting LiHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Mi-Wen ZhangHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Zhen-Zhou ZhangHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; State Key Laboratory of Medical Genomics & Shanghai Institute of Hypertension, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China.
Yu-Dan CaoDepartment of endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Xiao-Yan LiuHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Ran MiaoMedical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Yuan XuDepartment of endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Xiao-Fang SongDepartment of endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Jia-Wei SongHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Ying LiuHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Ying-Le XuState Key Laboratory of Medical Genomics & Shanghai Institute of Hypertension, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China.
Jing LiHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Ying DongHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Jiu-Chang ZhongHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China; State Key Laboratory of Medical Genomics & Shanghai Institute of Hypertension, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China. Electronic address: jczhong@sina.com.
Capital Medical University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiotensin converting enzyme 2 (ACE2) has recently been identified as the functional receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent response for novel coronavirus disease 2019 (COVID-19). This study aimed to explore the roles of ACE2, apelin and sodium-glucose cotransporter 2 (SGLT2) in SARS-CoV-2-mediated cardiorenal damage. METHODS AND

resultsThe published RNA-sequencing datasets of cardiomyocytes infected with SARS-CoV-2 and COVID-19 patients were used. String, UMAP plots and single cell RNA sequencing data were analyzed to show the close relationship and distinct cardiorenal distribution patterns of ACE2, apelin and SGLT2. Intriguingly, there were decreases in ACE2 and apelin expression as well as marked increases in SGLT2 and endothelin-1 levels in SARS-CoV-2-infected cardiomyocytes, animal models with diabetes, acute kidney injury, heart failure and COVID-19 patients. These changes were linked with downregulated levels of interleukin (IL)-10, superoxide dismutase 2 and catalase as well as upregulated expression of profibrotic genes and pro-inflammatory cytokines/chemokines. Genetic ACE2 deletion resulted in upregulation of pro-inflammatory cytokines containing IL-1β, IL-6, IL-17 and tumor necrosis factor α. More importantly, dapagliflozin strikingly alleviated cardiorenal fibrosis in diabetic db/db mice by suppressing SGLT2 levels and potentiating the apelin-ACE2 signaling.

conclusionDownregulation of apelin and ACE2 and upregulation of SGLT2, endothelin-1 and pro-inflammatory cytokines contribute to SARS-CoV-2-mediated cardiorenal injury, indicating that the apelin-ACE2 signaling and SGLT2 inhibitors are potential therapeutic targets for COVID-19 patients.

Indexed as

COVID-19Angiotensin-Converting Enzyme 2AnimalsApelinHumansMicePeptidyl-Dipeptidase ASARS-CoV-2Sodium-Glucose Transporter 2Angiotensin-Converting Enzyme 2ApelinPeptidyl-Dipeptidase ASodium-Glucose Transporter 2Angiotensin converting enzyme 2ApelinCOVID-19InflammationSevere acute respiratory syndrome coronavirus 2SGLT2 inhibitor

Identifiers

PMID34000358
PMCPMC8123373
OpenAlexW3162311882

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.