Evidence map›Paper›PMID 38369950›Full record

ArticleESC heart failure2024

Chlorogenic acid attenuates cardiac hypertrophy via up-regulating Sphingosine-1-phosphate receptor1 to inhibit endoplasmic reticulum stress.

Ping Ping, Ting Yang, Chaoxue Ning, Qingkai Zhao, Yali Zhao, Tao Yang, Zhitao Gao, Shihui Fu

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Ping PingGeneral Station for Drug and Instrument Supervision and Control, Joint Logistic Support Force of Chinese People's Liberation Army, Beijing, China.
Ting YangCentral Laboratory, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya, China.
Chaoxue NingCentral Laboratory, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya, China.
Qingkai ZhaoDepartment of Health and Medicine, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya, China.
Yali ZhaoCentral Laboratory, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya, China.
Tao YangDepartment of Oncology, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya, China.
Zhitao GaoSchool of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Shihui FuDepartment of Cardiology, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya, China.ORCID https://orcid.org/0000-0001-6707-9049
Hainan 301 Hospital · CNChinese General Hospital College of Nursing and Liberal Arts · PHGeneral Administration of Quality Supervision, Inspection and Quarantine · CNXinxiang Medical University · CN

Funding

2021 Military Training Injury Prevention Treatment Research Task 21xls37Excellent Youth Incubation Program of Chinese People's Liberation Army General Hospital 2020-YQPY-007Heatstroke Treatment and Research Center of PLA 413EGZ1D10Major Science and Technology Programme of Hainan Province ZDKJ2019012National Key R&D Program of China 2018YFC2000400National S&T Resource Sharing Service Platform Project of China YCZYPT[2018]07Natural Science Foundation of Hainan Province 820MS124Natural Science Foundation of Hainan Province 820MS126Natural Science Foundation of Hainan Province 820QN383Natural Science Foundation of Hainan Province 821MS112Natural Science Foundation of Hainan Province 821MS117Natural Science Foundation of Hainan Province 821QN389Natural Science Foundation of Hainan Province 822MS198Natural Science Foundation of Hainan Province 823MS161Sanya Medical and Health Science and Technology Innovation Project 2016YW21Sanya Medical and Health Science and Technology Innovation Project 2018YW10Sanya Medical and Health Science and Technology Innovation Project 2018YW11Sanya Medical and Health Science and Technology Innovation Project 2019YW12Simulation Training for Treatment of Heat StrokeSpecific Research Fund of Innovation Platform for Academicians of Hainan Province YSPTZX202216
6 · The paper itself

Abstract

aimsCardiac hypertrophy, an adaptive response of the heart to stress overload, is closely associated with heart failure and sudden cardiac death. This study aimed to investigate the therapeutic effects of chlorogenic acid (CGA) on cardiac hypertrophy and elucidate the underlying mechanisms. METHODS AND

resultsTo simulate cardiac hypertrophy, myocardial cells were exposed to isoproterenol (ISO, 10 μM). A rat model of ISO-induced cardiac hypertrophy was also established. The expression levels of cardiac hypertrophy markers, endoplasmic reticulum stress (ERS) markers, and apoptosis markers were measured using quantitative reverse transcription PCR and western blotting. The apoptosis level, size of myocardial cells, and heart tissue pathological changes were determined by terminal deoxynucleotidyl transferase dUTP nick-end labelling staining, immunofluorescence staining, haematoxylin and eosin staining, and Masson's staining. We found that CGA treatment decreased the size of ISO-treated H9c2 cells. Moreover, CGA inhibited ISO-induced up-regulation of cardiac hypertrophy markers (atrial natriuretic peptide, brain natriuretic peptide, and β-myosin heavy chain), ERS markers (C/EBP homologous protein, glucose regulatory protein 78, and protein kinase R-like endoplasmic reticulum kinase), and apoptosis markers (bax and cleaved caspase-12/9/3) but increased the expression of anti-apoptosis marker bcl-2 in a dose-dependent way (0, 10, 50, and 100 μM). Knockdown of sphingosine-1-phosphate receptor 1 (S1pr1) reversed the protective effect of CGA on cardiac hypertrophy, ERS, and apoptosis in vitro (P < 0.05). CGA also restored ISO-induced inhibition on the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) signalling in H9c2 cells, while S1pr1 knockdown abolished these CGA-induced effects (P < 0.05). CGA (90 mg/kg/day, for six consecutive days) protected rats against cardiac hypertrophy in vivo (P < 0.05).

conclusionsCGA treatment attenuated ISO-induced ERS and cardiac hypertrophy by activating the AMPK/SIRT1 pathway via modulation of S1pr1.

Indexed as

CardiomegalyChlorogenic AcidEndoplasmic Reticulum StressSphingosine-1-Phosphate ReceptorsUp-RegulationAnimalsApoptosisBlotting, WesternCells, CulturedDisease Models, AnimalMyocytes, CardiacRatsRats, Sprague-DawleySignal TransductionChlorogenic AcidS1PR1 protein, ratSphingosine-1-Phosphate ReceptorsCardiac hypertrophyChlorogenic acid (CGA)Endoplasmic reticulum stressSphingosine‐1‐phosphate receptor 1 (S1pr1)

Identifiers

PMID38369950
PMCPMC11098655
OpenAlexW4391928101

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.