Evidence map›Paper›PMID 42818311›Full record

ArticlebioRxiv : the preprint server for biology2026

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD.

Xinting Yu, Pinzhu Huang, Arvo Justice, Aaron Hakim, Yoshiko Nanki, Zaur Abilov, Edward B O'Neill, Jerry Cruz Rodriguez, Enzo Cabrera, Marla Sagatelian and 6 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Xinting YuDepartment of Internal Medicine, University of South Florida, Tampa, FL.ORCID 0000-0002-7497-0101
Pinzhu HuangDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Arvo JusticeDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Aaron HakimDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Yoshiko NankiDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Zaur AbilovDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Edward B O'NeillDepartment of Pathology and Cell Biology, University of South Florida, Tampa, FL.
Jerry Cruz RodriguezDepartment of Internal Medicine, University of South Florida, Tampa, FL.
Enzo CabreraDepartment of Pathology and Cell Biology, University of South Florida, Tampa, FL.
Marla SagatelianDepartment of Internal Medicine, University of South Florida, Tampa, FL.
Chandra S ShankarDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Brenda R FlamDepartment of Internal Medicine, University of South Florida, Tampa, FL.
Kawtar Al KhalloufiDepartment of Gastroenterology and Hepatology, Liver Transplant, Tampa General Hospital, University of South Florida, Tampa, FL.
Hiromi SesakiDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Shisong RongOcular Genomics Institute, Mass Eye and Ear, Harvard Medical School, Mass General Brigham, Boston, MA.
Yury V PopovDepartment of Medicine, Division of Gastroenterology, Hepatology & Nutrition, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.ORCID 0000-0001-7973-942X

Funding

Structure, Turnover and Safeguard of MitochondriaR35GM144103 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI Hiromi Sesaki · 2022 to 2026
$2.8M
Mitochondrial DAMPs-driven Mechanisms of Liver Fibrosis in NASHR01DK139288 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Yury Popov · 2024 to 2026
$2.0M
Role of DNAJC22 in Steatotic Liver DiseaseK08DK149008 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Aaron Hakim · 2026 to 2026
$164k
NIDDK NIH HHS K08 DK149008NIDDK NIH HHS R01 DK139288NIGMS NIH HHS R35 GM144103
6 · The paper itself

Abstract

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (

Identifiers

PMID42818311
PMCPMC13622249

What Socratic 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 Socratic graph.