Evidence map›Paper›PMID 21290324›Full record

ReviewAdvances in experimental medicine and biology2011

Molecular expression and functional role of canonical transient receptor potential channels in airway smooth muscle cells.

Yong-Xiao Wang, Yun-Min Zheng

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.1field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 29 citations in OpenAlex.

  1. Role of TRP channels in lymphatic function.Frontiers in physiology · 2026
    Review
  2. Review
  3. Histamine-induced cytosolic calcium mobilization in human bronchial smooth muscle cells.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025
    Article
  4. Review
  5. Article
  6. Mechanisms of BDNF regulation in asthmatic airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  7. Canonical transient receptor potential 3 channels activate NF-κB to mediate allergic airway disease via PKC-α/IκB-α and calcineurin/IκB-β pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  8. Article
  9. Article
  10. Neurokinin-neurotrophin interactions in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2011
    Article
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

2 authors at 1 institution in 1 country.

Yong-Xiao WangCenter for Cardiovascular Sciences, Albany Medical College, Albany, NY 12208, USA. wangy@mail.amc.edu
Yun-Min Zheng
Albany Medical Center Hospital · US

Funding

Novel Signaling for Ca2+ and Release in Airway MyocytesR01HL071000 · NHLBI · ALBANY MEDICAL COLLEGE · PI WANG, YONG-XIAO · 2003 to 2007
$1.8M
Signaling Mechanisms for Hypoxic Pulmonary VasoconstrictionR01HL108232 · NHLBI · ALBANY MEDICAL COLLEGE · PI WANG, YONG-XIAO · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL071000NHLBI NIH HHS R01HL071000NHLBI NIH HHS R01 HL108232
6 · The paper itself

Abstract

Multiple canonical or classic transient receptor potential (TRPC) molecules are expressed in animal and human airway smooth muscle cells (SMCs). TRPC3, but not TRPC1, is a major molecular component of native non-selective cation channels (NSCCs) to contribute to the resting [Ca(2+)](i) and muscarinic increase in [Ca(2+)](i) in freshly isolated airway SMCs. TRPC3-encoded NSCCs are significantly increased in expression and activity in airway SMCs from ovalbumin-sensitized/challenged "asthmatic" mice, whereas TRPC1-encoded channel activity, but not its expression, is largely augmented. The upregulated TRPC3- and TRPC1-encoded NSCC activity both mediate "asthmatic" membrane depolarization in airway SMCs. Supportively, tumor necrosis factor-α (TNFα), an important asthma mediator, increases TRPC3 expression, and TRPC3 gene silencing inhibits TNFα-mediated augmentation of acetylcholine-evoked increase in [Ca(2+)](i) in passaged airway SMCs. In contrast, TRPC6 gene silencing has no effect on 1-oleoyl-2-acetyl-sn-glycerol (OAG)-evoked increase in [Ca(2+)](i) in primary isolated cells. These findings provide compelling information indicating that TRPC3-encoded NSCCs are important for physiological and pathological cellular responses in airway SMCs. However, continual studies are necessary to further determine whether, which, and how TRPC-encoded channels are involved in cellular responses in normal and diseased (e.g., asthmatic) airway SMCs.

Indexed as

AnimalsCalciumIon TransportMembrane PotentialsMiceMuscle, SmoothTracheaTransient Receptor Potential ChannelsCalciumTransient Receptor Potential Channels

Identifiers

PMID21290324
PMCPMC3788176
OpenAlexW2159174899

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.