Evidence map›Paper›PMID 36195937›Full record

ArticleJournal of nanobiotechnology2022

Heart-targeting exosomes from human cardiosphere-derived cells improve the therapeutic effect on cardiac hypertrophy.

Liang Mao, Yun-Da Li, Ruo-Lan Chen, Gang Li, Xiao-Xia Zhou, Fei Song, Chan Wu, Yu Hu, Yi-Xiang Hong, Xitong Dang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Endogenous Engineering Reprograms Extracellular Vesicles for Enhanced Therapeutic Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

12 authors at 2 institutions in 1 country.

Liang MaoXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Yun-Da LiXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Ruo-Lan ChenXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Gang LiXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Xiao-Xia ZhouXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Fei SongXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Chan WuXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Yu HuXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Yi-Xiang HongXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Xitong DangKey Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention of Cardiovascular Diseases, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, 646000, China.
Gui-Rong LiXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.
Yan WangXiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China. wy@xmu.edu.cn.
First Affiliated Hospital of Xiamen University · CNSouthwest Medical University · CN

Funding

Grant from Central Government for Local Development of Science and Technology of Sichuan Province of China 2020ZYD047Grant from Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease of Sichuan Province of China xtcx2019-15Luzhou-Southwest Medical University joint scientific funding of China 2018LZXNYD-ZK25National Natural Science Foundation of China 81700268National Natural Science Foundation of China U1605226Special Supporting Foundation for Young Scientists of Southwest Medical University of China 2021-2023
6 · The paper itself

Abstract

Exosomes of human cardiosphere-derived cells (CDCs) are very promising for treating cardiovascular disorders. However, the current challenge is inconvenient delivery methods of exosomes for clinical application. The present study aims to explore the potential to enhance the therapeutic effect of exosome (EXO) from human CDCs to myocardial hypertrophy. A heart homing peptide (HHP) was displayed on the surface of exosomes derived from CDCs that were forced to express the HHP fused on the N-terminus of the lysosomal-associated membrane protein 2b (LAMP2b). The cardiomyocyte-targeting capability of exosomes were analyzed and their therapeutic effects were evaluated in a mouse model of myocardial hypertrophy induced by transverse aorta constriction (TAC). The molecular mechanisms of the therapeutic effects were dissected in angiotensin II-induced neonatal rat cardiomyocyte (NRCMs) hypertrophy model using a combination of biochemistry, immunohistochemistry and molecular biology techniques. We found that HHP-exosomes (HHP-EXO) accumulated more in mouse hearts after intravenous delivery and in cultured NRCMs than control exosomes (CON-EXO). Cardiac function of TAC mice was significantly improved with intravenous HHP-EXO administration. Left ventricular hypertrophy was reduced more by HHP-EXO than CON-EXO via inhibition of β-MHC, BNP, GP130, p-STAT3, p-ERK1/2, and p-AKT. Similar results were obtained in angiotensin II-induced hypertrophy of NRCMs, in which the beneficial effects of HHP-EXO were abolished by miRNA-148a inhibition. Our results indicate that HHP-EXO preferentially target the heart and improve the therapeutic effect of CDCs-exosomes on cardiac hypertrophy. The beneficial therapeutic effect is most likely attributed to miRNA-148a-mediated suppression of GP130, which in turn inhibits STAT3/ERK1/2/AKT signaling pathway, leading to improved cardiac function and remodeling.

Indexed as

ExosomesMicroRNAsAngiotensin IIAnimalsCardiomegalyCytokine Receptor gp130HumansLysosomal Membrane ProteinsMiceMyocytes, CardiacPeptidesProto-Oncogene Proteins c-aktRatsAngiotensin IICytokine Receptor gp130Lysosomal Membrane ProteinsMicroRNAsPeptidesProto-Oncogene Proteins c-aktCardiac hypertrophyCardiosphere-derived cellsExosomesGenetic engineeringHeart homing peptide

Identifiers

PMID36195937
PMCPMC9531502
OpenAlexW4300860262

What OpenQuestion 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 OpenQuestion graph.