Evidence map›Paper›PMID 33042446›Full record

ArticleAmerican journal of translational research2020

Qiliqiangxin prevents right ventricular remodeling by inhibiting apoptosis and improving metabolism reprogramming with pulmonary arterial hypertension.

Yingdong Lu, Jing Wu, Yuchan Sun, Laiyun Xin, Zhilin Jiang, Hongchen Lin, Mingjing Zhao, Xiangning Cui

Abstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Trial
  2. Article
  3. Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026
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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

8 authors.

Yingdong LuDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.
Jing WuDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.
Yuchan SunDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.
Laiyun XinDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.
Zhilin JiangDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.
Hongchen LinDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.
Mingjing ZhaoThe Key Laboratory of Chinese Internal Medicine of The Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese Medicine Beijing, China.
Xiangning CuiDepartment of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathological remodeling of the right ventricular (RV) contributes to the mortality of pulmonary arterial hypertension (PAH) patients, and RV myocardial apoptosis and metabolism play decisive roles in RV remodeling. Qiliqiangxin (QLQX), a traditional Chinese medicine, has a cardio-protective effective on left ventricular remodeling. However, whether QLQX can decrease RV myocardial apoptosis, improve metabolism, and attenuate RV remodeling remain uncertain. This study investigated the effects of QLQX on RV remodeling, myocardial mitochondria, apoptosis, and metabolism reprogramming. RV remodeling was induced by intraperitoneal injection of Monocrotaline (MCT). We first discovered that QLQX improved hemodynamic parameters and inhibited MCT-induced RVH. Next, QLQX significantly attenuated RV remodeling which covered RV myocardial fibrosis, and RV capillary density. Furthermore, we uncovered that QLQX attenuated RV myocardial apoptosis. We also confirmed that QLQX reversed metabolic shift toward glycolysis which decreased the uptake of glucose showed by fluorodeoxyglucose F 18 positron emission tomography (18FDG-PET). Mechanistically, QLQX optimized mitochondrial function by ameliorating structural abnormality of mitochondria, reducing the release of cytochrome c from mitochondria, and upregulating the expression of SOD2. Mitochondria-dependent apoptosis and mitochondria-associated metabolism were involved in QLQX regulation of RV. Moreover, our study showed that PINK1/Parkin 2 pathway was involved in improving mitochondrial function. We concluded that QLQX could inhibit PAH-induced RV remodeling by decreasing mitochondria associated apoptotic pathway and reversing mitochondrial related metabolic shift. The PINK1/Parkin mitophagy pathway may play a key role in mitochondria protection.

Indexed as

apoptosismetabolic shiftmitochondria functionmitophagypulmonary arterial hypertensionRight ventricular remodeling

Identifiers

PMID33042446
PMCPMC7540132

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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.