Evidence map›Paper›PMID 33242203›Full record

ArticleCardiovascular drugs and therapy2021

Extracellular Vesicles Derived from Intermittent Hypoxia-Treated Red Blood Cells Impair Endothelial Function Through Regulating eNOS Phosphorylation and ET-1 Expression.

Lu Peng, Yu Li, Xinwei Li, Yunhui Du, Linyi Li, Chaowei Hu, Jing Zhang, Yanwen Qin, Yongxiang Wei, Huina Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular drugs and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Systematic review of changes in extracellular vesicles associated with obstructive sleep apnoea: implications for diagnosis and treatment.European respiratory review : an official journal of the European Respiratory Society · 2025
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Nocturia and obstructive sleep apnoea.Nature reviews. Urology · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. The Effect of Extracellular Vesicles on Thrombosis.Journal of cardiovascular translational research · 2023
    Review
  10. Review
  11. Article
  12. Review
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  15. Article
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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

10 authors at 1 institution in 1 country.

Lu PengKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Yu LiKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Xinwei LiKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Yunhui DuKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Linyi LiKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Chaowei HuKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Jing ZhangKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Yanwen QinKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China.
Yongxiang WeiDepartment of Otolaryngology-Head and Neck Surgery, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China. wei__yongxiang@126.com.
Huina ZhangKey Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029, China. whinnerzhn@126.com.ORCID 0000-0003-1547-9926
Capital Medical University · CN

Funding

National Natural Science Foundation of China 81870335Natural Science Foundation of Beijing Municipality 7192031
6 · The paper itself

Abstract

purposeIntermittent hypoxia (IH), a main characteristic of obstructive sleep apnea (OSA) syndrome, has been known as a dominant cause of OSA-related endothelial dysfunction and hypertension. However, the underlying mechanism still remains unclear. Extracellular vesicles (EVs), small vesicles secreted by various cells, can be absorbed by endothelial cells and then influence vascular function. The aim of this research is to clarify whether and how EVs shedding from red blood cells (RBCs) are involved in IH-induced endothelial dysfunction.

methodsEVs were extracted by ultracentrifugation. After the identification of property and purity, EVs from IH-exposed RBCs (IH REVs) and normoxia-exposed RBCs (NOR REVs) or from OSA and non-OSA patient RBCs were utilized to treat C57BL/6 mouse aortas or human umbilical vein endothelial cells (HUVECs) for mechanistic exploration.

resultsFunctional results demonstrated that REVs from OSA patients dramatically impaired endothelium-dependent relaxations (EDRs). Similarly, in vivo and ex vivo studies showed that IH REVs caused significant endothelial dysfunction compared to control group. Further results presented that IH REVs blocked endothelial nitric oxide synthase (eNOS) phosphorylation through inhibiting PI3K/Akt pathway and enhanced endothelin-1 (ET-1) expression through activating Erk1/2 pathway in endothelial cells. Meanwhile, endothelial dysfunction caused by IH REVs was reversed by Akt activator SC79 as well as Erk kinase inhibitor PD98059, suggesting that PI3K/Akt/eNOS and Erk1/2/ET-1 pathways were implicated in IH REV-induced impaired EDRs.

conclusionsThis study reveals a novel role of REVs in endothelial dysfunction under IH and dissects the relevant mechanism involved in this process, which will help to establish a comprehensive understanding of OSA or IH-related endothelial dysfunction from a new scope.

Indexed as

AnimalsAortaEndothelin-1ErythrocytesExtracellular VesiclesHumansHuman Umbilical Vein Endothelial CellsHypoxiaMaleMiceMice, Inbred C57BLNitric Oxide Synthase Type IIIPhosphorylationEndothelin-1Nitric Oxide Synthase Type IIIEndothelial dysfunctionExtracellular vesicleIntermittent hypoxiaObstructive sleep apneaRed blood cell

Identifiers

PMID33242203
OpenAlexW3109526983

What Socratic holds

Textmetadata
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.