Evidence map›Paper›PMID 36685263›Full record

ArticleClinical and experimental hepatology2022

Cellular and mitochondrial taurine depletion in bile duct ligated rats: a justification for taurine supplementation in cholestasis/cirrhosis.

Asma Najibi, Heresh Rezaei, Ram Kumar Manthari, Hossein Niknahad, Akram Jamshidzadeh, Omid Farshad, Feng Yan, Yanqin Ma, Dongmei Xu, Zhongwei Tang and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Clinical and experimental hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 13 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

12 authors at 3 institutions in 3 countries.

Asma NajibiPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Heresh RezaeiDepartment of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
Ram Kumar ManthariDepartment of Biotechnology, GITAM Institute of Science, Gandhi Institute of Technology and Management, Visakhapatnam, Andhra Pradesh, India.
Hossein NiknahadPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Akram JamshidzadehPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Omid FarshadPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Feng YanDepartment of Life Sciences, Shanxi Agricultural University, Shanxi, Taigu, China.
Yanqin MaDepartment of Life Sciences, Shanxi Agricultural University, Shanxi, Taigu, China.
Dongmei XuDepartment of Life Sciences, Shanxi Agricultural University, Shanxi, Taigu, China.
Zhongwei TangDepartment of Life Sciences, Shanxi Agricultural University, Shanxi, Taigu, China.
Mohammad Mehdi OmmatiCollege of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Reza HeidariPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Shiraz University of Medical Sciences · IRShanxi Agricultural University · CNGITAM University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Taurine (TAU) is a free amino acid abundant in the human body. Various physiological roles have been attributed to TAU. At the subcellular level, mitochondria are the primary targets for TAU function. Meanwhile, it has been found that TAU depletion is associated with severe pathologies. Cholestasis is a severe clinical complication that can progress to liver fibrosis, cirrhosis, and hepatic failure. Bile duct ligation (BDL) is a reliable model for assessing cholestasis/cirrhosis and related complications. The current study was designed to investigate the effects of cholestasis/cirrhosis on tissue and mitochondrial TAU reservoirs. Cholestatic rats were monitored (14 and 42 days after BDL surgery), and TAU levels were assessed in various tissues and isolated mitochondria. There was a significant decrease in TAU in the brain, heart, liver, kidney, skeletal muscle, intestine, lung, testis, and ovary of the BDL animals (14 and 42 days after surgery). Mitochondrial levels of TAU were also significantly depleted in BDL animals. Tissue and mitochondrial TAU levels in cirrhotic animals (42 days after the BDL operation) were substantially lower than those in the cholestatic rats (14 days after BDL surgery). These data indicate an essential role for tissue and mitochondrial TAU in preventing organ injury induced by cholestasis/cirrhosis and could justify TAU supplementation for therapeutic purposes.

Indexed as

amino acidbile acidscirrhosismitochondrial impairmentoxidative stress

Identifiers

PMID36685263
PMCPMC9850306
OpenAlexW4296639001

What Socratic holds

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LicenceCC BY-NC-SA
Read underepoch 390

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 Socratic graph.