Evidence map›Paper›PMID 38851078›Full record

ArticleRedox biology2024

Sweroside alleviates pressure overload-induced heart failure through targeting CaMKⅡδ to inhibit ROS-mediated NF-κB/NLRP3 in cardiomyocytes.

Dong Wang, Xue Yu, Kuo Gao, Fanghe Li, Xiang Li, Haiyin Pu, Peng Zhang, Shuzhen Guo, Wei Wang

Abstract read
In one paragraph

Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–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

32 citing papers in PubMed.

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  19. Article
  20. c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
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

9 authors.

Dong WangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China.
Xue YuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China.
Kuo GaoSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China.
Fanghe LiSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China.
Xiang LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 102488, China.
Haiyin PuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China.
Peng ZhangWuhan Hospital of Traditional Chinese Medicine, Wuhan, 430014, China. Electronic address: zhangpengcxm@sohu.com.
Shuzhen GuoSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. Electronic address: guoshz@bucm.edu.cn.
Wei WangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. Electronic address: wangwei26960@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ongoing inflammation in the heart is positively correlated with adverse remodeling, characterized by elevated levels of cytokines that stimulate activation of cardiac fibroblasts. It was found that CaMKIIδ response to Ang II or TAC triggers the accumulation of ROS in cardiomyocytes, which subsequently stimulates NF-κB/NLRP3 and leads to an increase in IL-6, IL-1β, and IL-18. This is an important causative factor in the occurrence of adverse remodeling in heart failure. Sweroside is a biologically active natural iridoids extracted from Lonicerae Japonicae Flos. It shows potent anti-inflammatory and antioxidant activity in various cardiovascular diseases. In this study, we found that sweroside inhibited ROS-mediated NF-κB/NLRP3 in Ang II-treated cardiomyocytes by directly binding to CaMKIIδ. Knockdown of CaMKⅡδ abrogated the effect of sweroside regulation on NF-κB/NLRP3 in cardiomyocytes. AAV-CaMKⅡδ induced high expression of CaMKⅡδ in the myocardium of TAC/Ang II-mice, and the inhibitory effect of sweroside on TAC/Ang Ⅱ-induced elevation of NF-κB/NLRP3 was impeded. Sweroside showed significant inhibitory effects on CaMKIIδ/NF-κB/NLRP3 in cardiomyocytes from TAC/Ang Ⅱ-induced mice. This would be able to mitigate the adverse events of myocardial remodeling and contractile dysfunction at 8 weeks after the onset of the inflammatory response. Taken together, our findings have revealed the direct protein targets and molecular mechanisms by which sweroside improves heart failure, thereby supporting the further development of sweroside as a therapeutic agent for heart failure.

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase Type 2Heart FailureMyocytes, CardiacNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesAnimalsDisease Models, AnimalMaleMiceSignal TransductionCalcium-Calmodulin-Dependent Protein Kinase Type 2NF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesCardiac remodelingCardiomyocytesHeart failureInflammationSweroside

Identifiers

PMID38851078
PMCPMC11219961

What OpenQuestion holds

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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.