Evidence map›Paper›PMID 23142761›Full record

ArticleDevelopmental biology2013

Absence of venous valves in mice lacking Connexin37.

Stephanie J Munger, John D Kanady, Alexander M Simon

Abstract read
In one paragraph

Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Endothelial Connexins in Developmental and Pathological Angiogenesis.Cold Spring Harbor perspectives in medicine · 2022
    Review
  6. Review
  7. Connexin Expression Is Altered in Liver Development ofInternational journal of molecular sciences · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Mechanisms of Connexin-Related Lymphedema.Circulation research · 2018
    Article
  15. Connexins and Pannexins in Vascular Function and Disease.International journal of molecular sciences · 2018
    Review
  16. Pannexin-1 in Human Lymphatic Endothelial Cells Regulates Lymphangiogenesis.International journal of molecular sciences · 2018
    Article
  17. Article
  18. Review
  19. Human venous valve disease caused by mutations in FOXC2 and GJC2.The Journal of experimental medicine · 2017
    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

3 authors at 1 institution in 1 country.

Stephanie J MungerDepartment of Physiology, University of Arizona, Tucson, AZ 85724, USA. sjmunger@email.arizona.edu
John D Kanady
Alexander M Simon
University of Arizona · US

Funding

PHYSIOLOGYT32HL007249 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson, JOHN P KONHILAS · 1985 to 2026
$12.5M
Gap Junction Mediated Signaling and Vascular ResponsesR01HL064232 · NHLBI · UNIVERSITY OF ARIZONA · PI SIMON, ALEXANDER M · 2001 to 2010
$2.2M
NHLBI NIH HHS R01 HL064232NHLBI NIH HHS R01-HL64232NHLBI NIH HHS T32 HL007249NHLBI NIH HHS T32-HL007249
6 · The paper itself

Abstract

Venous valves play a crucial role in blood circulation, promoting the one-way movement of blood from superficial and deep veins towards the heart. By preventing retrograde flow, venous valves spare capillaries and venules from being subjected to damaging elevations in pressure, especially during skeletal muscle contraction. Pathologically, valvular incompetence or absence of valves are common features of venous disorders such as chronic venous insufficiency and varicose veins. The underlying causes of these conditions are not well understood, but congenital venous valve aplasia or agenesis may play a role in some cases. Despite progress in the study of cardiac and lymphatic valve morphogenesis, the molecular mechanisms controlling the development and maintenance of venous valves remain poorly understood. Here, we show that in valved veins of the mouse, three gap junction proteins (Connexins, Cxs), Cx37, Cx43, and Cx47, are expressed exclusively in the valves in a highly polarized fashion, with Cx43 on the upstream side of the valve leaflet and Cx37 on the downstream side. Surprisingly, Cx43 expression is strongly induced in the non-valve venous endothelium in superficial veins following wounding of the overlying skin. Moreover, we show that in Cx37-deficient mice, venous valves are entirely absent. Thus, Cx37, a protein involved in cell-cell communication, is one of only a few proteins identified so far as critical for the development or maintenance of venous valves. Because Cxs are necessary for the development of valves in lymphatic vessels as well, our results support the notion of common molecular pathways controlling valve development in veins and lymphatic vessels.

Indexed as

AnimalsConnexin 43ConnexinsEndotheliumExtremitiesGap Junction alpha-4 ProteinMiceMice, Inbred C57BLProtein TransportRegional Blood FlowSaphenous VeinSkinVenous ValvesConnexin 43connexin 47ConnexinsGap Junction alpha-4 Protein

Identifiers

PMID23142761
PMCPMC3533519
OpenAlexW2016676019

What OpenQuestion holds

Textmetadata
LicenceTDM
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.