Evidence map›Paper›PMID 31547195›Full record

ArticleCells2019

Serine Protease HtrA2/Omi Deficiency Impairs Mitochondrial Homeostasis and Promotes Hepatic Fibrogenesis via Activation of Hepatic Stellate Cells.

Wonhee Hur, Byung Yoon Kang, Sung Min Kim, Gil Won Lee, Jung-Hee Kim, Min-Kyung Nam, Hyangshuk Rhim, Seung Kew Yoon

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. [Research Progress on the Role of Mitochondrial DNA in the Pathogenesis of Chronic Liver Disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Article
  10. Article
  11. Dissecting the role of interprotomer cooperativity in the activation of oligomeric high-temperature requirement A2 protein.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. 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

8 authors at 1 institution in 1 country.

Wonhee HurCatholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Byung Yoon KangCatholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Sung Min KimCatholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Gil Won LeeCatholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Jung-Hee KimCatholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
Min-Kyung NamDepartment of Biomedicine and Health Sciences, College of Medicine, The Catholic University of Korea, , Seoul 06591, Korea.
Hyangshuk RhimDepartment of Biomedicine and Health Sciences, College of Medicine, The Catholic University of Korea, , Seoul 06591, Korea.
Seung Kew YoonCatholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea. yoonsk@catholic.ac.kr.
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The loss of mitochondrial function impairs intracellular energy production and potentially results in chronic liver disease. Increasing evidence suggests that mitochondrial dysfunction in hepatocytes contributes to the activation of hepatic stellate cells (HSCs), thereby resulting in hepatic fibrogenesis. High-temperature requirement protein A2 (HtrA2/Omi), a mitochondrial serine protease with various functions, is responsible for quality control in mitochondrial homeostasis. However, little information is available regarding its role in mitochondrial damage during the development of liver fibrosis. This study examined whether HtrA2/Omi regulates mitochondrial homeostasis in hepatocyte during the development of hepatic fibrogenesis. In this study, we demonstrated that HtrA2/Omi expression considerably decreased in liver tissues from the CCl

Indexed as

AnimalsCells, CulturedDisease ProgressionHepatic Stellate CellsHigh-Temperature Requirement A Serine Peptidase 2HomeostasisHumansLiver CirrhosisMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicMitochondriaOxidative StressReactive Oxygen SpeciesHigh-Temperature Requirement A Serine Peptidase 2HTRA2 protein, humanHtra2 protein, mouseReactive Oxygen Specieshepatic fibrogenesisHtrA2/Omimitochondrial functionmitochondrial homeostasisreactive oxygen species stress

Identifiers

PMID31547195
PMCPMC6829542
OpenAlexW2973550463

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.