Evidence map›Paper›PMID 41581151›Full record

ArticleCell reports2026

Scar-associated endothelial-stellate cellular crosstalk drives fibrosis resolution in MASH.

Kenneth Li, Vardhman Kumar, Tran To, Álvaro González-Domínguez, Janvi Huria, Maylene Yu, Bruno Cogliati, Chittampalli N Yashaswini, Mark Miller, Andrea D Branch and 8 more

Abstract read
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. CombinedFrontiers in pharmacology · 2026
    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

18 authors.

Kenneth LiDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Mount Sinai Institute for Liver Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Vardhman KumarKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Tran ToDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Álvaro González-DomínguezDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Janvi HuriaKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA; Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, MA, USA.
Maylene YuDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Bruno CogliatiDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Chittampalli N YashaswiniDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Mark MillerDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Andrea D BranchDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Bruno GiottiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Alexander M TsankovDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Li ChenPharmaNest, Inc., Princeton, NJ, USA.
Mathieu PetitjeanPharmaNest, Inc., Princeton, NJ, USA.
Jesse D KirkpatrickKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA; Harvard University-Massachusetts Institute of Technology Division of Health Sciences and Technology, Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA.
Sangeeta N BhatiaKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA; Harvard University-Massachusetts Institute of Technology Division of Health Sciences and Technology, Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA; Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, MA, USA; Marble Center for Cancer Nanomedicine, Massachusetts Institute of Technology, Cambridge, MA, USA; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA; Wyss Institute at Harvard University, Boston, MA, USA; Howard Hughes Medical Institute, Cambridge, MA, USA.
Scott L FriedmanDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Mount Sinai Institute for Liver Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Shuang WangDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Mount Sinai Institute for Liver Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: shuang.wang@mssm.edu.

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
MOUNT SINAI MEDICAL SCIENTIST TRAINING PROGRAMT32GM007280 · NIGMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BARON, MARGARET H · 1985 to 2021
$22.8M
TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
Hepatic stellate cells in NASH fibrosis and HCCR01DK128289 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SCOTT L. FRIEDMAN · 2021 to 2026
$2.6M
Hepatic stellate cell plasticity and maladaptive fibrogenic memory in chronic liver diseaseR01DK136016 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Shuang Wang · 2023 to 2026
$2.3M
NCI NIH HHS P30 CA196521NCI NIH HHS T32 CA078207NIDDK NIH HHS R01 DK128289NIDDK NIH HHS R01 DK136016NIGMS NIH HHS T32 GM007280
6 · The paper itself

Abstract

Fibrosis contributes to ∼40% of mortality in the industrialized world. Fibrosis in the liver can spontaneously resolve when injury terminates. In this study, we establish a robust mouse model of fibrosis regression in MASH (metabolic dysfunction-associated steatohepatitis), a highly prevalent chronic liver disease worldwide, and perform single-cell and in situ molecular profiling to define the molecular drivers of fibrosis regression. Prediction of cell-cell communication identifies a Wnt9b-Sfrp2 crosstalk that emerges as fibrosis resolves, the perturbation of which attenuates spontaneous fibrosis regression. We further identify a subset of liver endothelial cells termed "Endo4" as the source of Wnt9b. Immunostaining for the Endo4 marker VWF using tissue clearing and 3D imaging reveals VWF+ vasculature juxtaposing activated hepatic stellate cells that penetrate deep into the fibrotic septa and exhibit in situ protease activity, establishing them as de facto scar-associated endothelial cells and a regulatory node in murine MASH fibrosis regression.

Indexed as

CicatrixEndothelial CellsHepatic Stellate CellsLiver CirrhosisAnimalsCell CommunicationDisease Models, AnimalLiverMiceMice, Inbred C57BLCP: metabolismendo-stellate crosstalkfibrosis regressionin situ protease activityliver endothelial cellsMASH mouse modelscar-associated endothelial cellsscar-associated nichesingle-cell/nucleus RNA sequencingtissue clearing and 3D imagingWNT signaling

Identifiers

PMID41581151
PMCPMC13010457

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.