Evidence map›Paper›PMID 31033175›Full record

ArticleJournal of cellular and molecular medicine2019

Chlorogenic acid: A potent molecule that protects cardiomyocytes from TNF-α-induced injury via inhibiting NF-κB and JNK signals.

Lei Tian, Cong-Ping Su, Qing Wang, Fu-Jian Wu, Rui Bai, Hui-Min Zhang, Jin-Ying Liu, Wen-Jing Lu, Wei Wang, Feng Lan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 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

11 authors at 2 institutions in 1 country.

Lei TianSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Cong-Ping SuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Qing WangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Fu-Jian WuBeijing Laboratory for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Rui BaiBeijing Laboratory for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Hui-Min ZhangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Jin-Ying LiuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Wen-Jing LuBeijing Laboratory for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Wei WangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Feng LanBeijing Laboratory for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-9038-4014
Shu-Zhen GuoSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.ORCID 0000-0002-8980-9812
Beijing University of Chinese Medicine · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The traditional Chinese herb Lonicerae Japonicae Flos has shown significant clinical benefits in the treatment of heart failure, but the mechanism remains unclear. As the main active ingredient found in the plasma after oral administration of Lonicerae Japonicae Flos, chlorogenic acid (CGA) has been reported to possess anti-inflammatory, anti-oxidant and anti-apoptosis function. We firstly confirmed the cardioprotective effects of CGA in transverse aortic constriction (TAC)-induced heart failure mouse model, through mitigating the TNF-α-induced toxicity. We further used TNF-α-induced cardiac injury in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to elucidate the underlying mechanisms. CGA pre-treatment could reverse TNF-α-induced cellular injuries, including improved cell viability, increased mitochondrial membrane potential and inhibited cardiomyocytes apoptosis. We then examined the NF-κB/p65 and major mitogen-activated protein kinases (MAPKs) signalling pathways involved in TNF-α-induced apoptosis of hiPSC-CMs. Importantly, CGA can directly inhibit NF-κB signal by suppressing the phosphorylation of NF-κB/p65. As for the MAPKs, CGA suppressed the activity of only c-Jun N-terminal kinase (JNK), but enhanced extracellular signal-regulated kinase1/2 (ERK1/2) and had no effect on p38. In summary, our study revealed that CGA has profound cardioprotective effects through inhibiting the activation of NF-κB and JNK pathway, providing a novel therapeutic alternative for prevention and treatment of heart failure.

Indexed as

AnimalsAortaApoptosisCardiotonic AgentsCell SurvivalChlorogenic AcidConstriction, PathologicCytoprotectionDisease Models, AnimalHeart FailureInduced Pluripotent Stem CellsMaleMAP Kinase Signaling SystemMice, Inbred C57BLModels, BiologicalMyocytes, CardiacCardiotonic AgentsChlorogenic AcidNF-kappa BTumor Necrosis Factor-alphaapoptosischlorogenic acidhiPSC-CMstumour necrosis factor-α

Identifiers

PMID31033175
PMCPMC6584503
OpenAlexW2943411383

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.