Evidence map›Paper›PMID 37828006›Full record

ArticleSignal transduction and targeted therapy2023

Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression.

Yan Liu, Yi-Hui Shao, Jun-Meng Zhang, Ying Wang, Mei Zhou, Hui-Qin Li, Cong-Cong Zhang, Pei-Jie Yu, Shi-Juan Gao, Xue-Rui Wang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 35 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

14 authors at 4 institutions in 2 countries.

Yan Liu *Beijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Yi-Hui Shao *Beijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Jun-Meng ZhangBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Ying WangBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Mei ZhouBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Hui-Qin LiBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Cong-Cong ZhangBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Pei-Jie YuBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Shi-Juan GaoBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Xue-Rui WangBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Li-Xin JiaBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Chun-Mei PiaoBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Jie DuBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
Yu-Lin LiBeijing Anzhen Hospital, Capital Medical University; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Collaborative Innovative Research Center for Cardiovascular Diseases; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China. lyllyl_1111@163.com.
Beijing Anzhen Hospital · CNMinistry of Education · ROBeijing Institute of Water · CNCapital Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81300120National Natural Science Foundation of China (National Science Foundation of China) 81430050National Natural Science Foundation of China (National Science Foundation of China) 81770250Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) Z200026
6 · The paper itself

Abstract

Immune cell infiltration in response to myocyte death regulates extracellular matrix remodeling and scar formation after myocardial infarction (MI). Caspase-recruitment domain family member 9 (CARD9) acts as an adapter that mediates the transduction of pro-inflammatory signaling cascades in innate immunity; however, its role in cardiac injury and repair post-MI remains unclear. We found that Card9 was one of the most upregulated Card genes in the ischemic myocardium of mice. CARD9 expression increased considerably 1 day post-MI and declined by day 7 post-MI. Moreover, CARD9 was mainly expressed in F4/80-positive macrophages. Card9 knockout (KO) led to left ventricular function improvement and infarct scar size reduction in mice 28 days post-MI. Additionally, Card9 KO suppressed cardiomyocyte apoptosis in the border region and attenuated matrix metalloproteinase (MMP) expression. RNA sequencing revealed that Card9 KO significantly suppressed lipocalin 2 (Lcn2) expression post-MI. Both LCN2 and the receptor solute carrier family 22 member 17 (SL22A17) were detected in macrophages. Subsequently, we demonstrated that Card9 overexpression increased LCN2 expression, while Card9 KO inhibited necrotic cell-induced LCN2 upregulation in macrophages, likely through NF-κB. Lcn2 KO showed beneficial effects post-MI, and recombinant LCN2 diminished the protective effects of Card9 KO in vivo. Lcn2 KO reduced MMP9 post-MI, and Lcn2 overexpression increased Mmp9 expression in macrophages. Slc22a17 knockdown in macrophages reduced MMP9 release with recombinant LCN2 treatment. In conclusion, our results demonstrate that macrophage CARD9 mediates the deterioration of cardiac function and adverse remodeling post-MI via LCN2.

Indexed as

Heart InjuriesMyocardial InfarctionAnimalsCARD Signaling Adaptor ProteinsLipocalin-2MacrophagesMatrix Metalloproteinase 9MiceCard9 protein, mouseCARD Signaling Adaptor ProteinsLipocalin-2Matrix Metalloproteinase 9

Identifiers

PMID37828006
PMCPMC10570328
OpenAlexW4387566743

What OpenQuestion holds

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LicenceCC BY
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.