Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage

Inmaculada Ruz-Maldonado, John T. Gonzalez, Hanming Zhang, Jonathan Sun, Alicia Bort, Inamul Kabir, Richard G. Kibbey, Yajaira Suárez, Daniel M. Greif and Carlos Fernández-Hernando ()
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Inmaculada Ruz-Maldonado: Yale University School of Medicine
John T. Gonzalez: Yale University School of Medicine
Hanming Zhang: Yale University School of Medicine
Jonathan Sun: Yale University School of Medicine
Alicia Bort: Yale University School of Medicine
Inamul Kabir: Yale University School of Medicine
Richard G. Kibbey: Yale University School of Medicine
Yajaira Suárez: Yale University School of Medicine
Daniel M. Greif: Yale University School of Medicine
Carlos Fernández-Hernando: Yale University School of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-23

Abstract: Abstract Midlobular hepatocytes are proposed to be the most plastic hepatic cell, providing a reservoir for hepatocyte proliferation during homeostasis and regeneration. However, other mechanisms beyond hyperplasia have been little explored and the contribution of other hepatocyte subpopulations to regeneration has been controversial. Thus, re-examining hepatocyte dynamics during regeneration is critical for cell therapy and treatment of liver diseases. Using a mouse model of hepatocyte- and non-hepatocyte- multicolor lineage tracing, we demonstrate that midlobular hepatocytes also undergo hypertrophy in response to chemical, physical, and viral insults. Our study shows that this subpopulation also combats liver impairment after infection with coronavirus. Furthermore, we demonstrate that pericentral hepatocytes also expand in number and size during the repair process and Galectin-9-CD44 pathway may be critical for driving these processes. Notably, we also identified that transdifferentiation and cell fusion during regeneration after severe injury contribute to recover hepatic function.

Date: 2024
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DOI: 10.1038/s41467-024-45439-0

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