Evidence map›Paper›PMID 35456592›Full record

ReviewPharmaceutics2022

Designer Functional Nanomedicine for Myocardial Repair by Regulating the Inflammatory Microenvironment.

Chunping Liu, Zhijin Fan, Dongyue He, Huiqi Chen, Shihui Zhang, Sien Guo, Bojun Zheng, Huan Cen, Yunxuan Zhao, Hongxing Liu and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. KLF9 deficiency protects the heart from inflammatory injury triggered by myocardial infarction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Article
  9. Review
  10. 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

11 authors at 3 institutions in 2 countries.

Chunping LiuGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Zhijin FanMolecular Diagnosis and Treatment Center for Infectious Diseases, Dermatology Hospital, Southern Medical University, Guangzhou 510091, China.ORCID 0000-0003-0018-4949
Dongyue HeGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Huiqi ChenGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Shihui ZhangGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Sien GuoGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Bojun ZhengGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Huan CenGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Yunxuan ZhaoGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.
Hongxing LiuDepartment of Urology, Guangzhou Institute of Urology, Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510230, China.ORCID 0000-0002-0723-5529
Lei WangState Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.ORCID 0000-0001-5349-6298
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Guangzhou Medical University · CNSouthern Medical University · CN

Funding

2020-2021 Achievement and clinical transformation seedling Project of the First Affiliated Hospital of Guangzhou Medical University ZH202108Fund of Science and Technology Innovation Strategy of Guangdong Province 191900105Guangdong Basic and Applied Basic Research Foundation 2021A1515012573 and 2019A1515111108Guangdong Province Medical Research Fund A2021033Macau Young Scholars Program AM2021023National Natural Science Foundation of China 82104495,82174161,82002253, &82102083Research Fund of State Key Laboratory of Dampness Syndrome of Chinese Medicine SZ2021ZZ21Science and Technology Foundation of Guangzhou City 202102010257Scientific research projects of Guangdong Bureau of traditional Chinese Medicine 20200513093851TCM Research Fund of Guangdong Provincial Hospital of Chinese Medicine YN2019MJ15
6 · The paper itself

Abstract

Acute myocardial infarction is a major global health problem, and the repair of damaged myocardium is still a major challenge. Myocardial injury triggers an inflammatory response: immune cells infiltrate into the myocardium while activating myofibroblasts and vascular endothelial cells, promoting tissue repair and scar formation. Fragments released by cardiomyocytes become endogenous "danger signals", which are recognized by cardiac pattern recognition receptors, activate resident cardiac immune cells, release thrombin factors and inflammatory mediators, and trigger severe inflammatory responses. Inflammatory signaling plays an important role in the dilation and fibrosis remodeling of the infarcted heart, and is a key event driving the pathogenesis of post-infarct heart failure. At present, there is no effective way to reverse the inflammatory microenvironment in injured myocardium, so it is urgent to find new therapeutic and diagnostic strategies. Nanomedicine, the application of nanoparticles for the prevention, treatment, and imaging of disease, has produced a number of promising applications. This review discusses the treatment and challenges of myocardial injury and describes the advantages of functional nanoparticles in regulating the myocardial inflammatory microenvironment and overcoming side effects. In addition, the role of inflammatory signals in regulating the repair and remodeling of infarcted hearts is discussed, and specific therapeutic targets are identified to provide new therapeutic ideas for the treatment of myocardial injury.

Indexed as

inflammatory microenvironmentmolecular imagingmyocardial repairnanomedicine

Identifiers

PMID35456592
PMCPMC9025700
OpenAlexW4220813419

What Socratic holds

Textmetadata
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 Socratic graph.