Evidence map›Paper›PMID 27610009›Full record

ArticleWorld journal of gastroenterology2016

Mitochondrial DNA from hepatocytes as a ligand for TLR9: Drivers of nonalcoholic steatohepatitis?

Priya Handa, Akhila Vemulakonda, Kris V Kowdley, Misael Uribe, Nahum Méndez-Sánchez

Open access · hybridAbstract readEditorial
In one paragraph

Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  17. Innate immune regulatory networks in hepatic lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2019
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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

5 authors at 2 institutions in 2 countries.

Priya HandaPriya Handa, Akhila Vemulakonda, Kris V Kowdley, Senior Research Scientist, Organ Care Research and Liver Care Network, Swedish Medical Center, Seattle, WA 98104, United States.
Akhila VemulakondaPriya Handa, Akhila Vemulakonda, Kris V Kowdley, Senior Research Scientist, Organ Care Research and Liver Care Network, Swedish Medical Center, Seattle, WA 98104, United States.
Kris V KowdleyPriya Handa, Akhila Vemulakonda, Kris V Kowdley, Senior Research Scientist, Organ Care Research and Liver Care Network, Swedish Medical Center, Seattle, WA 98104, United States.
Misael UribePriya Handa, Akhila Vemulakonda, Kris V Kowdley, Senior Research Scientist, Organ Care Research and Liver Care Network, Swedish Medical Center, Seattle, WA 98104, United States.
Nahum Méndez-SánchezPriya Handa, Akhila Vemulakonda, Kris V Kowdley, Senior Research Scientist, Organ Care Research and Liver Care Network, Swedish Medical Center, Seattle, WA 98104, United States.
Swedish Medical Center · USHospital Médica Sur · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, affecting approximately one third of the Western world. It consists of a wide spectrum of liver disorders, ranging from fatty liver to nonalcoholic steatohepatitis (NASH), which consists of steatosis, ballooning injury and inflammation. Despite an alarming growth in the statistics surrounding NAFLD, there are as yet no effective therapies for its treatment. Innate immune signaling has been thought to play a significant role in initiating and augmenting hepatic inflammation, contributing to the transition from nonalcoholic fatty liver to NASH. An immune response is triggered by countless signals called damage-associated molecular patterns (DAMPs) elicited by lipid-laden and damaged hepatocytes, which are recognized by pattern recognition receptors (PRRs) on hepatic immune cells to initiate inflammatory signaling. In this editorial, in addition to summarizing innate immune signaling in NAFLD and discussing potential therapies that target innate immune pathways, we have described a recent study that demonstrated that mitochondrial DNA serves as a DAMP activating a hepatic PRR, TLR9, in mice and in the plasma of NASH patients. In addition to identifying a new ligand for TLR9 during NASH progression, the study shows that blocking TLR9 reverses NASH, paving the way for the development of future NASH therapy.

Indexed as

AnimalsDNA, MitochondrialHepatocytesHumansImmunity, InnateLigandsMiceNon-alcoholic Fatty Liver DiseaseToll-Like Receptor 9DNA, MitochondrialLigandsToll-Like Receptor 9Damage-associated molecular patternsHepatocytesInflammationInnate immune signalingKupffer cellsMitochondrial DNANonalcoholic fatty liver diseaseNonalcoholic steatohepatitisProducts of microbial metabolism produced by pathogensTherapyTLR9

Identifiers

PMID27610009
PMCPMC4988306
OpenAlexW2509664072

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.