Evidence map›Paper›PMID 36082934›Full record

ArticleActa biochimica et biophysica Sinica2022

A novel lncRNA FPASL regulates fibroblast proliferation via the PI3K/AKT and MAPK signaling pathways in hypertrophic scar.

Fang Ma, Jiangyong Shen, Hui Zhang, Zhenghao Zhang, Anning Yang, Jiantuan Xiong, Yun Jiao, Zhigang Bai, Shengchao Ma, Huiping Zhang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Fang MaSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Jiangyong ShenNHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, China.
Hui ZhangSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Zhenghao ZhangSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Anning YangSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Jiantuan XiongSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Yun JiaoNHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, China.
Zhigang BaiNHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, China.
Shengchao MaSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Huiping ZhangNHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, China.
Yideng JiangSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Ningxia Medical University · CNNingxia Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic scar is a problem for numerous patients, especially after burns, and is characterized by increased fibroblast proliferation and collagen deposition. Increasing evidence demonstrates that lncRNAs contribute to the development and progression of various diseases. However, the function of lncRNAs in hypertrophic scar formation remains poorly characterized. In this study, a novel fibroblast proliferation-associated lncRNA, named lncRNA FPASL (MSTRG.389905.1), which is mainly localized in the cytoplasm, is found to be downregulated in hypertrophic scar, as detected by lncRNA microarray and qRT-PCR. The full-length FPASL is characterized and further investigation confirms that it has no protein-coding potential. FPASL knockdown in fibroblasts triggers fibroblast proliferation, whereas overexpression of FPASL directly attenuates the proliferation of fibroblasts. Furthermore, target genes of the differentially expressed lncRNAs in hypertrophic scars and the matched adjacent normal tissues are enriched in fibroblast proliferation signaling pathways, including the PI3K/AKT and MAPK signaling pathways, as determined by GO annotation and KEGG enrichment analysis. We also demonstrate that knockdown of FPASL activates the PI3K/AKT and MAPK signaling pathways, and specific inhibitors of the PI3K/AKT and MAPK signaling pathways can reverse the proliferation of fibroblasts promoted by FPASL knockdown. Our findings contribute to a better understanding of the role of lncRNAs in hypertrophic scar and suggest that FPASL may act as a potential novel therapeutic target for hypertrophic scar.

Indexed as

Cicatrix, HypertrophicRNA, Long NoncodingCell ProliferationFibroblastsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long Noncodingfibroblasthypertrophic scarlncRNA FPASLMAPKPI3K/AKT

Identifiers

PMID36082934
PMCPMC10157618
OpenAlexW4293660586

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.