Evidence map›Paper›PMID 33788198›Full record

ArticleAdvances in experimental medicine and biology2021

Cytokines, Chemokines, and Inflammation in Pulmonary Arterial Hypertension.

Shuxin Liang, Ankit A Desai, Stephen M Black, Haiyang Tang

Abstract read
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In one paragraph

Article in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
54.6field-weighted citation impact, top 1% 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

22 citing papers in PubMed, 46 citations in OpenAlex.

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  7. Lymphocyte Involvement in the Pathology of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2024
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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

4 authors at 4 institutions in 2 countries.

Shuxin LiangCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Ankit A DesaiDepartment of Medicine, Indiana University, Indianapolis, IN, USA.
Stephen M BlackDivision of Translational and Regenerative Medicine, College of Medicine, University of Arizona, Tucson, AZ, USA.
Haiyang TangCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China. tanghy2008@yahoo.com.
First Affiliated Hospital of Guangzhou Medical University · CNGuangzhou Medical University · CNIndiana University – Purdue University Indianapolis · USUniversity of Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

According to the World Symposium Pulmonary Hypertension (WSPH) classification, pulmonary hypertension (PH) is classified into five categories based on etiology. Among them, Group 1 pulmonary arterial hypertension (PAH) disorders are rare but progressive and often, fatal despite multiple approved treatments. Elevated pulmonary arterial pressure in patients with WSPH Group 1 PAH is mainly caused by increased pulmonary vascular resistance (PVR), due primarily to sustained pulmonary vasoconstriction and excessive obliterative pulmonary vascular remodeling. Growing evidence indicates that inflammation plays a critical role in the development of pulmonary vascular remodeling associated with PAH. While the role of auto-immunity is unclear, infiltration of inflammatory cells in and around vascular lesions, including T- and B-cells, dendritic cells, macrophages, and mast cells have been observed in PAH patients. Serum and plasma levels of chemokines, cytokines, and autoantibodies are also increased in PAH patients; some of these circulating molecules are correlated with disease severity and survival. Preclinical experiments have reported a key role of the inflammation in PAH pathophysiology in vivo. Importantly, anti-inflammatory and immunosuppressive agents have further exhibited therapeutic effects. The present chapter reviews published experimental and clinical evidence highlighting the canonical role of inflammation in the pathogenesis of PAH and as a major target for the development of anti-inflammatory therapies in patients with PAH.

Indexed as

Pulmonary Arterial HypertensionChemokinesCytokinesFamilial Primary Pulmonary HypertensionHumansInflammationPulmonary ArteryChemokinesCytokinesAnti-inflammatory and immunosuppressive agentsInflammationPulmonary arterial hypertension

Identifiers

PMID33788198
OpenAlexW3145855414

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.