Hepatic stellate cells control liver zonation, size and functions via R-spondin 3

A Atsushi Sugimoto Y Yoshinobu Saito G Guanxiong Wang Q Qiuyan Sun C Chuan Yin K Ki Hong Lee Y Yana Geng P Presha Rajbhandari C Celine Hernandez M Marcella Steffani J Jingran Qie T Thomas Savage D Dhruv M. Goyal K Kevin C. Ray T Taruna V. Neelakantan D Deqi Yin J Johannes Melms B Brandon M. Lehrich T Tyler M. Yasaka S Silvia Liu M Michael Oertel T Tian Lan A Adrien Guillot M Moritz Peiseler A Aveline Filliol H Hiroaki Kanzaki N Naoto Fujiwara S Samhita Ravi B Benjamin Izar M Mario Brosch J Jochen Hampe H Helen Remotti J Josepmaria Argemí Z Zhaoli Sun T Timothy J. Kendall Y Yujin Hoshida F Frank Tacke J Jonathan A. Fallowfield S Storm K. Blockley-Powell R Rebecca A. Haeusler J Jonathan B. Steinman U Utpal B. Pajvani S Satdarshan P. Monga R Ramon Bataller M Mojgan Masoodi N Nicholas Arpaia Y Youngmin A. Lee B Brent R. Stockwell H Hellmut G. Augustin R Robert F. Schwabe

Abstract

Abstract Hepatic stellate cells (HSCs) have a central pathogenetic role in the development of liver fibrosis. However, their fibrosis-independent and homeostatic functions remain poorly understood1–5. Here we demonstrate that genetic depletion of HSCs changes WNT activity and zonation of hepatocytes, leading to marked alterations in liver regeneration, cytochrome P450 metabolism and injury. We identify R-spondin 3 (RSPO3), an HSC-enriched modulator of WNT signalling, as responsible for these hepatocyte-regulatory effects of HSCs. HSC-selective deletion of Rspo3 phenocopies the effects of HSC depletion on hepatocyte gene expression, zonation, liver size, regeneration and cytochrome P450-mediated detoxification, and exacerbates alcohol-associated and metabolic dysfunction-associated steatotic liver disease. RSPO3 expression decreases with HSC activation and is inversely associated with outcomes in patients with alcohol-associated and metabolic dysfunction-associated steatotic liver disease. These protective and hepatocyte-regulating functions of HSCs via RSPO3 resemble the R-spondin-expressing stromal niche in other organs and should be integrated into current therapeutic concepts.

Article Details

Journal Nature
Volume / Issue Vol. 640, Issue 8059
Published April 17, 2025
Pages 752-761
ISSN 0028-0836
Publisher Nature Portfolio

Journal Info

Nature

Nature Portfolio

ISSN: 0028-0836 Health Sciences

Authors (50)

A

Atsushi Sugimoto

Y

Yoshinobu Saito

G

Guanxiong Wang

Q

Qiuyan Sun

C

Chuan Yin

K

Ki Hong Lee

Y

Yana Geng

P

Presha Rajbhandari

C

Celine Hernandez

M

Marcella Steffani

J

Jingran Qie

T

Thomas Savage

D

Dhruv M. Goyal

K

Kevin C. Ray

T

Taruna V. Neelakantan

D

Deqi Yin

J

Johannes Melms

B

Brandon M. Lehrich

T

Tyler M. Yasaka

S

Silvia Liu

M

Michael Oertel

T

Tian Lan

A

Adrien Guillot

M

Moritz Peiseler

A

Aveline Filliol

H

Hiroaki Kanzaki

N

Naoto Fujiwara

S

Samhita Ravi

B

Benjamin Izar

M

Mario Brosch

J

Jochen Hampe

H

Helen Remotti

J

Josepmaria Argemí

Z

Zhaoli Sun

T

Timothy J. Kendall

Y

Yujin Hoshida

F

Frank Tacke

J

Jonathan A. Fallowfield

S

Storm K. Blockley-Powell

R

Rebecca A. Haeusler

J

Jonathan B. Steinman

U

Utpal B. Pajvani

S

Satdarshan P. Monga

R

Ramon Bataller

M

Mojgan Masoodi

N

Nicholas Arpaia

Y

Youngmin A. Lee

B

Brent R. Stockwell

H

Hellmut G. Augustin

R

Robert F. Schwabe