Evidence map›Paper›PMID 35744848›Full record

ReviewMolecules (Basel, Switzerland)2022

Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension.

Dan Xu, Ya-Hui Hu, Xue Gou, Feng-Yang Li, Xi-Yu-Chen Yang, Yun-Man Li, Feng Chen

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
9.3field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. DNA damage and arterial hypertension. A systematic review and meta-analysis.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 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

7 authors at 3 institutions in 1 country.

Dan XuState Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, China.
Ya-Hui HuDepartment of Pharmacy, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Xue GouState Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, China.
Feng-Yang LiKey Laboratory of Chemical Biology (Ministry of Education), Department of Pharmacology, School of Pharmaceutical Sciences, Shandong University, Jinan 250000, China.
Xi-Yu-Chen YangState Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, China.
Yun-Man LiState Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, China.
Feng ChenDepartment of Pharmacy, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
China Pharmaceutical University · CNSecond Affiliated Hospital of Nanjing Medical University · CNShandong University · CN

Funding

the Medical Science and Technique Foundation of Nanjing Health Commission YKK19104the National Major Scientific and Technological Special Project for "Significant New Drugs Development" during the Thirteenth Five-year Plan Period 2018ZX09301043-001the Natural Science Foundation of China 82073845the Specially Appointed Medical Expert Project of Jiangsu Commission of Health 2019
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is clinically characterized by a progressive increase in pulmonary artery pressure, followed by right ventricular hypertrophy and subsequently right heart failure. The underlying mechanism of PAH includes endothelial dysfunction and intimal smooth muscle proliferation. Numerous studies have shown that oxidative stress is critical in the pathophysiology of PAH and involves changes in reactive oxygen species (ROS), reactive nitrogen (RNS), and nitric oxide (NO) signaling pathways. Disrupted ROS and NO signaling pathways cause the proliferation of pulmonary arterial endothelial cells (PAECs) and pulmonary vascular smooth muscle cells (PASMCs), resulting in DNA damage, metabolic abnormalities, and vascular remodeling. Antioxidant treatment has become a main area of research for the treatment of PAH. This review mainly introduces oxidative stress in the pathogenesis of PAH and antioxidative therapies and explains why targeting oxidative stress is a valid strategy for PAH treatment.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionAnimalsAntioxidantsCell ProliferationDisease Models, AnimalEndothelial CellsMyocytes, Smooth MuscleOxidative StressPulmonary ArteryReactive Oxygen SpeciesAntioxidantsReactive Oxygen Speciesendothelial dysfunctionoxidative stresspulmonary arterial hypertensiontherapeutic strategy

Identifiers

PMID35744848
PMCPMC9229274
OpenAlexW4282565626

What Socratic 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 Socratic graph.