Evidence map›Paper›PMID 30878663›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

Senescent Hepatocytes in Decompensated Liver Show Reduced UPR

Bijoya Sen, Archana Rastogi, Rhisita Nath, Saggere M Shasthry, Viniyendra Pamecha, Sonika Pandey, Kapuganti Jagadis Gupta, Shiv K Sarin, Nirupma Trehanpati, Gayatri Ramakrishna

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. [Research progress on cellular senescence and liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  2. Article
  3. p16Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Exploring Cirrhosis: Insights into Advances in Therapeutic Strategies.International journal of molecular sciences · 2025
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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

10 authors at 2 institutions in 1 country.

Bijoya SenDepartment of Molecular and Cellular Medicine, Institute of Liver and Biliary Sciences, New Delhi, India.
Archana RastogiDepartment of Pathology, Institute of Liver and Biliary Sciences, New Delhi, India.
Rhisita NathDepartment of Molecular and Cellular Medicine, Institute of Liver and Biliary Sciences, New Delhi, India.
Saggere M ShasthryDepartment of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India.
Viniyendra PamechaDepartment of Hepato-Pancreato-Biliary and Liver Transplant Surgery, Institute of Liver and Biliary Sciences, New Delhi, India.
Sonika PandeyNational Institute of Plant Genome Research, New Delhi, India.
Kapuganti Jagadis GuptaNational Institute of Plant Genome Research, New Delhi, India.
Shiv K SarinDepartment of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India.
Nirupma TrehanpatiDepartment of Molecular and Cellular Medicine, Institute of Liver and Biliary Sciences, New Delhi, India.
Gayatri RamakrishnaDepartment of Molecular and Cellular Medicine, Institute of Liver and Biliary Sciences, New Delhi, India. Electronic address: rgayatri@ilbs.in.
Institute of Liver and Biliary Sciences · INNational Institute of Plant Genome Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsNon-dividing hepatocytes in end-stage liver disease indicates permanent growth arrest similar to senescence. Identifying senescence in vivo is often challenging and mechanisms inhibiting senescence are poorly understood. In lower organisms mitochondrial unfolded protein response (UPR

methodsDoxorubicin was used to induce senescence in non-neoplastic hepatocytes (PH5CH8) and hepatoma cells (HepG2 and Huh7). Senescence-associated markers and unfolded protein response was evaluated by fluorescence microscopy, immunoblotting and gene expression. Explants/biopsies from normal, fibrosis, compensated and decompensated cirrhosis without any known etiology were examined for presence of senescence and UPR

resultsAccumulation of senescent hepatocytes in cryptogenic cirrhosis was associated with reduced proliferation, increased expression of γH2AX and p21, together with loss of LaminB1. Dysfunctional mitochondria and compromised UPR

conclusionsOur results implicate a role of hepatocyte senescence in cryptogenic cirrhosis together with a crucial role of UPR

Indexed as

AdultBiopsyCase-Control StudiesCell Line, TumorCell ProliferationCellular SenescenceDoxycyclineEndopeptidase ClpFemaleHepatocytesHep G2 CellsHumansIn Vitro TechniquesLiver CirrhosisMaleMiddle AgedClpP protein, humanDoxycyclineEndopeptidase ClpReactive Oxygen SpeciesCryptogenic Liver CirrhosisMitochondrial RespirationMitochondrial Unfolded Protein ResponseOxidative Stress

Identifiers

PMID30878663
PMCPMC6520637
OpenAlexW2921011959

What OpenQuestion holds

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Registered trials

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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.