Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

M1-like macrophage-derived exosomes suppress angiogenesis and exacerbate cardiac dysfunction in a myocardial infarction microenvironment.

Basic research in cardiology - 28 Feb 2020

Liu Shaojun, Chen Jing, Shi Jian, Zhou Wenyi, Wang Li, Fang Weilun, Zhong Yun, Chen Xiaohui, Chen Yanfang, Sabri Abdelkarim, Liu Shiming

Abstract excerpt

The roles and the underlying mechanisms of M1-type macrophages in angiogenesis and postmyocardial infarction (MI) cardiac repair have remained unclear. In this study, we investigated the role of M1-like macrophage-derived exosomes in a MI microenvironment. We found that the proinflammatory M1-like-type macrophages released an extensive array of proinflammatory exosomes (M1-Exos) after MI. M1-Exos exerted an...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cellular Microenvironment
Share to Exosomes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Neovascularization, Physiologic

Share to rab27 GTP-Binding Proteins

Share to RAW 264.7 Cells

Share to Sphingomyelin Phosphodiesterase

Share to THP-1 Cells

Share to Ventricular Function, Left

Source

Identifiers

PMID: 32112145
DOI: 10.1007/s00395-020-0781-7

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

M1-like macrophage-derived exosomes suppress angiogenesis and exacerbate cardiac dysfunction in a myocardial infarction microenvironment.PMID 32112145Read ↗

MiR-378a-3p Promotes Macrophage Polarization from M1 to M2 for Cardiac Repair after Infarction Via Trem1.Semantic proximity Read ↗

SHEP1 alleviates cardiac ischemia reperfusion injury via targeting G3BP1 to regulate macrophage infiltration and inflammationSemantic proximity Read ↗

Macrophage-Derived mir-155-Containing Exosomes Suppress Fibroblast Proliferation and Promote Fibroblast Inflammation during Cardiac InjurySemantic proximity Read ↗

M2 Macrophage Exosomes Reverse Cardiac Functional Decline in Mice with Diet-Induced Myocardial Infarction by Suppressing Type 1 Interferon Signaling in Myeloid CellsSemantic proximity Read ↗

Human umbilical cord mesenchymal stem cells derived Exosomes attenuate injury of myocardial infarction by miR-24-3p-promoted M2 macrophage polarizationSemantic proximity Read ↗

Macrophage Polarization as a Therapeutic Target in Myocardial Infarction.Semantic proximity Read ↗

OxLDL-Stimulated Macrophages Transmit Exosomal MicroRNA-320b to Aggravate Viability, Invasion, and Phenotype Switching via Regulating PPARGC1A-Mediated MEK/ERK Pathway in Proatherogenic Vascular Smooth Muscle Cells.Semantic proximity Read ↗

Chemokine-like receptor 1 deficiency impedes macrophage phenotypic transformation and cardiac repair after myocardial infarction.Semantic proximity Read ↗

Exosomal hsa_circ_0007047 Attenuates Pos-myocardial Infarction Remodeling by Promoting Angiogenesis via miR-1178-3p/PDPK1 AxisSemantic proximity Read ↗

CDC-derived extracellular vesicles reprogram inflammatory macrophages to an arginase 1-dependent proangiogenic phenotype.Semantic proximity Read ↗

Intervention of Tanshinone IIA on the PGK1-PDHK1 Pathway to Reprogram Macrophage Phenotype After Myocardial Infarction.Semantic proximity Read ↗

Angiogenesis after acute myocardial infarction.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.