Evidence map›Paper›PMID 36296961›Full record

ReviewNutrients2022

The Role and Mechanism of Gut Microbiota in Pulmonary Arterial Hypertension.

Yi-Hang Chen, Wen Yuan, Liu-Kun Meng, Jiu-Chang Zhong, Xiao-Yan Liu

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  17. Respiratory diseases and the gut microbiota: an updated review.Frontiers in cellular and infection microbiology · 2025
    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

5 authors at 2 institutions in 1 country.

Yi-Hang ChenHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Wen YuanMedical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Liu-Kun MengState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100032, China.
Jiu-Chang ZhongHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0002-2315-3515
Xiao-Yan LiuHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Capital Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

Beijing Hospitals Authority Youth Program QML20200305Beijing Natural Science Foundation 7222138, 7222068; 7162069National Major Research Plan Training Program of the National Natural Science Foundation of China No. 82170302, 82070325, 92168117; 81770253; 91849111Reform and Development Program of Beijing Institute of Respiratory Medicine ysrh2022010, ysrh2022002, ysrh2022007
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a malignant pulmonary vascular disease characterized by increased pulmonary vascular resistance, pulmonary vasoconstriction, and right ventricular hypertrophy. Recent developments in genomics and metabolomics have gradually revealed the roles of the gut microbiota (GM) and its metabolites in cardiovascular diseases. Accumulating evidence reveals that the GM plays important roles in the occurrence and development of PAH. Gut microbiota dysbiosis directly increases the gut permeability, thereby facilitating pathological bacterial translocation and allowing translocation of bacterial products such as lipopolysaccharides from the gut into circulation. This process aggravates pulmonary perivascular inflammation and exacerbates PAH development through the endothelial-mesenchymal transition. Additionally, a shift in the composition of PAH also affects the gut metabolites. Changes in gut metabolites, such as decreased short-chain fatty acids, increased trimethylamine N-oxide, and elevated serotonin, contribute to pulmonary perivascular inflammation and pulmonary vascular remodeling by activating several signaling pathways. Studies of the intestinal microbiota in treating pulmonary hypertension have strengthened linkages between the GM and PAH. Probiotic therapy and fecal microbiota transplantation may supplement existing PAH treatments. In this article, we provide new insight for diagnosing, preventing and treating PAH by adding to the current knowledge of the intestinal flora mechanisms and its metabolites efficacy involved in PAH.

Indexed as

Gastrointestinal MicrobiomeProbioticsPulmonary Arterial HypertensionDysbiosisFatty Acids, VolatileHumansInflammationLipopolysaccharidesSerotoninFatty Acids, VolatileLipopolysaccharidesSerotoningut microbiota dysbiosismetabolismmicrobiota transfer therapyprebiotics and probioticspulmonary arterial hypertensionpulmonary vascular remodeling

Identifiers

PMID36296961
PMCPMC9610674
OpenAlexW4306153461

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.