Evidence map›Paper›PMID 37606791›Full record

ArticleApplied microbiology and biotechnology2023

Application of recombinant TGF-β1 inhibitory peptide to alleviate isoproterenol-induced cardiac fibrosis.

Yufei Qiu, Xudong Song, Yong Liu, Yan Wu, Jiayi Shi, Fan Zhang, Yu Pan, Zhiqin Cao, Keke Zhang, Jingruo Liu and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Applied microbiology and biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. MCardiovascular diagnosis and therapy · 2024
    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

13 authors at 1 institution in 1 country.

Yufei Qiu *Heilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Xudong Song *Heilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Yong LiuHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Yan WuHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Jiayi ShiHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Fan ZhangHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Yu PanHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Zhiqin CaoHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Keke ZhangHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Jingruo LiuHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Yanhui ChuHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China.
Xiaohuan YuanHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China. yuanxiaohuan@mdjmu.edu.cn.
Dan WuHeilongjiang Province Key Laboratory of Anti-Fibrosis Biotherapy, Mudanjiang Medical University, No.3, Tongxiang Street, Aimin District, Mudanjiang, 157011, Heilongjiang, China. wudan@mdjmu.edu.cn.ORCID http://orcid.org/0000-0002-0241-4691
Mudanjiang Medical University · CN

Funding

Central Finance supports Local Colleges, and Universities Talent Development Funding from Heilongjiang Provincial Department of Finance (High Level Talent Support Project） 2020GSP09Doctoral Research Foundation of Mudanjiang Medical University 2021-MYBSKY-066Natural Science Foundation of Heilongjiang Province (Outstanding Youth Project) YQ2020H026Scientific research project of Health Commission of Heilongjiang Province 20220101040974Torch Program Youth Top Talent Project of Mudanjiang Medical University 2022-MYHJ-015
6 · The paper itself

Abstract

Cardiac fibrosis is a remodeling process of the cardiac interstitium, characterized by abnormal metabolism of the extracellular matrix, excessive accumulation of collagen fibers, and scar tissue hyperplasia. Persistent activation and transdifferentiation into myofibroblasts of cardiac fibroblasts promote the progression of fibrosis. Transforming growth factor-β1 (TGF-β1) is a pivotal factor in cardiac fibrosis. Latency-associated peptide (LAP) is essential for activating TGF-β1 and its binding to the receptor. Thus, interference with TGF-β1 and the signaling pathways using LAP may attenuate cardiac fibrosis. Recombinant full-length and truncated LAP were previously constructed, expressed, and purified. Their effects on cardiac fibrosis were investigated in isoproterenol (ISO)-induced cardiac fibroblasts (CFs) and C57BL/6 mice. The study showed that LAP and tLAP inhibited ISO-induced CF activation, inflammation, and fibrosis, improved cardiac function, and alleviated myocardial injury in ISO-induced mice. LAP and tLAP alleviated the histopathological alterations and inhibited the elevated expression of inflammatory and fibrosis-related markers in cardiac tissue. In addition, LAP and tLAP decreased the ISO-induced elevated expression of TGF-β, αvβ3, αvβ5, p-Smad2, and p-Smad3. The study indicated that LAP and tLAP attenuated ISO-induced cardiac fibrosis via suppressing TGF-β/Smad pathway. This study may provide a potential approach to alleviate cardiac fibrosis. KEY POINTS: • LAP and tLAP inhibited ISO-induced CF activation, inflammation, and fibrosis. • LAP and tLAP improved cardiac function and alleviated myocardial injury, inflammation, and fibrosis in ISO-induced mice. • LAP and tLAP attenuated cardiac fibrosis via suppressing TGF-β/Smad pathway.

Indexed as

FibrosisIsoproterenolPeptidesTransforming Growth Factor beta1AnimalsDisease Models, AnimalFibroblastsMaleMiceMice, Inbred C57BLMyocardiumRecombinant ProteinsSignal TransductionSmad ProteinsIsoproterenolPeptidesRecombinant ProteinsSmad ProteinsTransforming Growth Factor beta1Cardiac fibrosisIsoproterenolLatency-associated peptideTGF-β/Smad pathway

Identifiers

PMID37606791
OpenAlexW4386046937

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.