Evidence map›Paper›PMID 27194472›Full record

ArticleAmerican journal of physiology. Cell physiology2016

Sodium tanshinone IIA sulfonate inhibits hypoxia-induced enhancement of SOCE in pulmonary arterial smooth muscle cells via the PKG-PPAR-γ signaling axis.

Qian Jiang, Wenju Lu, Kai Yang, Cyrus Hadadi, Xin Fu, Yuqin Chen, Xin Yun, Jie Zhang, Meichan Li, Lei Xu and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  4. Review
  5. Review
  6. Review
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  9. Review
  10. Article
  11. Review
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  13. Article
  14. Article
  15. Review
  16. Article
  17. PPARPPAR research · 2018
    Article
  18. Article
  19. Article
  20. 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

14 authors at 7 institutions in 2 countries.

Qian JiangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Wenju LuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Kai YangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Cyrus HadadiDepartment of Cardiology, Geisinger Medical Center, Danville, Pennsylvania.
Xin FuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Yuqin ChenState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Xin YunState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Jie ZhangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Meichan LiState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;
Lei XuDepartment of Respiratory Diseases, The Affiliated Hospital of Inner Mongolia Medical University Hohhot, Inner Mongolia, China; and.
Haiyang TangDivision of Translational and Regenerative Medicine, Department of Medicine, The University of Arizona, Tucson, Arizona;
Jason X-J YuanDivision of Translational and Regenerative Medicine, Department of Medicine, The University of Arizona, Tucson, Arizona;
Jian WangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China; Division of Translational and Regenerative Medicine, Department of Medicine, The University of Arizona, Tucson, Arizona; Division of Pulmonary Medicine, The People's Hospital of Inner Mongolia, Hohhot, Inner Mongolia, China; jianwang1@email.arizona.edu.
Dejun SunDivision of Pulmonary Medicine, The People's Hospital of Inner Mongolia, Hohhot, Inner Mongolia, China;
State Key Laboratory of Respiratory Disease · CNFirst Affiliated Hospital of Guangzhou Medical University · CNGuangzhou Medical University · CNUniversity of Arizona · USGeisinger Medical Center · USInner Mongolia Medical University · CNInner Mongolia People's Hospital · CN

Funding

Role of Bone Morphogenetic Protein 4 in Hypoxic Pulmomary HypertensionR01HL093020 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI WANG, JIAN · 2010 to 2014
$1.8M
NHLBI NIH HHS R01 HL093020
6 · The paper itself

Abstract

Our laboratory previously showed that sodium tanshinone IIA sulfonate (STS) inhibited store-operated Ca(2+) entry (SOCE) through store-operated Ca(2+) channels (SOCC) via downregulating the expression of transient receptor potential canonical proteins (TRPC), which contribute to the formation of SOCC (Wang J, Jiang Q, Wan L, Yang K, Zhang Y, Chen Y, Wang E, Lai N, Zhao L, Jiang H, Sun Y, Zhong N, Ran P, Lu W. Am J Respir Cell Mol Biol 48: 125-134, 2013). The detailed molecular mechanisms by which STS inhibits SOCE and downregulates TRPC, however, remain largely unknown. We have previously shown that, under hypoxic conditions, inhibition of protein kinase G (PKG) and peroxisome proliferator-activated receptor-γ (PPAR-γ) signaling axis results in the upregulation of TRPC (Wang J, Yang K, Xu L, Zhang Y, Lai N, Jiang H, Zhang Y, Zhong N, Ran P, Lu W. Am J Respir Cell Mol Biol 49: 231-240, 2013). This suggests that strategies targeting the restoration of this signaling pathway may be an effective treatment strategy for pulmonary hypertension. In this study, our results demonstrated that STS treatment can effectively prevent the hypoxia-mediated inhibition of the PKG-PPAR-γ signaling axis in rat distal pulmonary arterial smooth muscle cells (PASMCs) and distal pulmonary arteries. These effects of STS treatment were blocked by pharmacological inhibition or specific small interfering RNA knockdown of either PKG or PPAR-γ. Moreover, targeted PPAR-γ agonist markedly enhanced the beneficial effects of STS. These results comprehensively suggest that STS treatment can prevent hypoxia-mediated increases in intracellular calcium homeostasis and cell proliferation, by targeting and restoring the hypoxia-inhibited PKG-PPAR-γ signaling pathway in PASMCs.

Indexed as

AnimalsCalcium SignalingCell ProliferationCells, CulturedCyclic GMP-Dependent Protein KinasesDisease Models, AnimalDose-Response Relationship, DrugHypertension, PulmonaryHypoxiaMaleMuscle, Smooth, VascularMyocytes, Smooth MusclePhenanthrenesPPAR gammaProtein Kinase InhibitorsPulmonary ArteryCyclic GMP-Dependent Protein KinasesPhenanthrenesPPAR gammaPPAR gamma, ratProtein Kinase Inhibitorstanshinone II A sodium sulfonatetransient receptor potential cation channel, subfamily C, member 1Trpc6 protein, ratTRPC Cation ChannelsPKGPPAR-γSOCESTSTRPC

Identifiers

PMID27194472
PMCPMC4967135
OpenAlexW2405536997

What OpenQuestion 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 OpenQuestion graph.