Evidence map›Paper›PMID 30904607›Full record

ArticleEBioMedicine2019

Mitochondrial dysfunction-mediated decline in angiogenic capacity of endothelial progenitor cells is associated with capillary rarefaction in patients with hypertension via downregulation of CXCR4/JAK2/SIRT5 signaling.

Bing-Bo Yu, Hui Zhi, Xiao-Yu Zhang, Jian-Wen Liang, Jiang He, Chen Su, Wen-Hao Xia, Gao-Xing Zhang, Jun Tao

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Endothelial Progenitor Cells: Disease Markers and Potential Therapy in Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025
    Review
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  8. Article
  9. Article
  10. Heliyon · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023
    Review
  18. Article
  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

9 authors at 2 institutions in 1 country.

Bing-Bo YuDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Hui ZhiDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Xiao-Yu ZhangDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Jian-Wen LiangDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Jiang HeDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Chen SuDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Wen-Hao XiaDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China.
Gao-Xing ZhangDepartment of Cardiovascular Disease, The Jiangmen Central Hospital, China. Electronic address: zhang.g.x@medmail.com.cn.
Jun TaoDepartment of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, China. Electronic address: taojungz123@163.com.
Sun Yat-sen University · CNJiangmen Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertensive patients exhibit decline in capillary density and endothelial progenitor cells (EPCs). However, whether capillary rarefaction in hypertension is associated with defect angiogenesis of EPCs remains unknown. We hypothesized that impaired mitochondrial function of late EPCs in hypertension is associated with the structural lack of capillary microcirculation via deficient CXCR4/JAK2/SIRT5 signaling.

methodsWe performed capillary microcirculation detection in hypertensive patients and healthy subjects. Angiogenic capacity and mitochondrial function of circulating EPCs were evaluated. The underlying mechanisms were further investigated by genetic inhibition and overexpression.

findingsCapillary density of nail fold and eye fundus were significantly reduced in hypertensive patients, which was paralleled to decreased in vitro late EPC function and in vivo angiogenic capacity. Meanwhile the decline of EPC function in hypertension was accompanied by impaired mitochondrial ultrastructure, diminished mitochondrial membrane potential, reduced oxygen consumption, increased ROS generation and NADH level. Rotenone induced inhibition of oxygen consumption rate, excessive ROS generation and loss of MMP, which markedly decreased the in vitro functions of EPCs. Furthermore, SIRT5 expression of EPCs in hypertension was markedly reduced, which was correlated to mitochondrial dysfunction. CXCR4 gene transfer enhanced SIRT5 expression, improved mitochondrial functions and augmented angiogenic capacity of EPCs. The beneficial impacts of SIRT5 up-regulation on late EPC-mediated angiogenesis can be abrogated by blockade of CXCR4/JAK2/SIRT5 signaling pathway.

interpretationMitochondrial dysfunction-mediated fall in angiogenic capacity due to deficient CXCR4/JAK2/SIRT5 signaling of late EPCs is probably responsible for the capillary rarefaction in hypertension. Our findings provide insight into the potential of EPC mitochondria as a novel target for the treatment of hypertension-related loss of microvascular density. FUNDS: National Nature Science Foundation of China, 973Program, the Nature Science Foundation of Guangdong.

Indexed as

Neovascularization, PhysiologicAnimalsBiomarkersDisease Models, AnimalEndothelial Progenitor CellsGene ExpressionHumansHypertensionJanus Kinase 2MaleMembrane Potential, MitochondrialMiceMicrovascular RarefactionMitochondriaModels, BiologicalOxygen ConsumptionBiomarkersCXCR4 protein, humanJAK2 protein, humanJanus Kinase 2Reactive Oxygen SpeciesReceptors, CXCR4SIRT5 protein, humanSirtuinsAngiogenesisCXCR4EPCsHypertensionMicrocirculationMitochondriaSIRT5

Identifiers

PMID30904607
PMCPMC6491423
OpenAlexW2924427905

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.