Apoptosis and necroptosis in the liver: a matter of life and death

Schwabe, Robert F.; Luedde, Tom

doi:10.1038/s41575-018-0065-y

Cited by 589Cell death mechanisms and regulationLiver physiology and pathologyLiver Disease Diagnosis and Treatment

Apoptosis and necroptosis in the liver: a matter of life and death

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Schwabe, Robert F., Luedde, Tom·2018·Nature Reviews Gastroenterology & Hepatology

DOI 10.1038/s41575-018-0065-yPMC PMC6490680

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Abstract

Cell death represents a basic biological paradigm that governs outcomes and long-term sequelae in almost every hepatic disease condition. Acute liver failure is characterized by massive loss of parenchymal cells but is usually followed by restitution ad integrum. By contrast, cell death in chronic liver diseases often occurs at a lesser extent but leads to long-term alterations in organ architecture and function, contributing to chronic hepatocyte turnover, the recruitment of immune cells and activation of hepatic stellate cells. These chronic cell death responses contribute to the development of liver fibrosis, cirrhosis and cancer. It has become evident that, besides apoptosis, necroptosis is a highly relevant form of programmed cell death in the liver. Differential activation of specific forms of programmed cell death might not only affect outcomes in liver diseases but also offer novel opportunities for therapeutic intervention. Here, we summarize the underlying molecular mechanisms and open questions about disease-specific activation and roles of programmed cell death forms, their contribution to response signatures and their detection. We focus on the role of apoptosis and necroptosis in acute liver injury, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH) and liver cancer, and possible translations into clinical applications.

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A key feature of MASH is hepatocyte apoptosis, which correlates with liver fibrosis.
“A key feature of MASH is hepatocyte apoptosis, which correlates with the clinically most important feature of the disease, liver fibrosis (6, 7).”
From Impaired TIM4-mediated efferocytosis by liver macrophages contributes to fibrosis in metabolic dysfunction–associated steatohepatitis (2025) · cites this paper as [6]
The “NASH and CLD” section says most data point to hepatocyte apoptosis as a key driver in NASH (now termed MASH). The “Fibroinflammation” section reports a correlation between apoptosis markers and fibrosis in patients, but does not establish that correlation specifically in MASH; the paper also discusses evidence that necroptosis may be important in NASH. Page numbers were unavailable in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measured
HSCs have fibrosis-independent roles through RSPO3, regulating critical parameters that affect CLD progression and outcomes, including metabolic hepatocyte functions, liver regeneration and hepatocyte death.
“The current study amends this fibrocentric concept by demonstrating fibrosis-independent roles for HSCs through RSPO3, regulating critical parameters that affect CLD progression and outcomes, including metabolic hepatocyte functions, liver regeneration and hepatocyte death2,49,50.”
From Hepatic stellate cells control liver zonation, size and functions via R-spondin 3 (2025) · cites this paper as [50]
The Introduction links chronic hepatocyte death to CLD complications, and the Regeneration section links chronic hepatocyte regeneration to replication-induced DNA damage. The cited paper does not establish that HSCs act through RSPO3 or that metabolic hepatocyte functions affect CLD progression; the citing sentence presents the HSC–RSPO3 finding as its own study’s result. No page numbers are available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Apoptosis of hepatocytes is a central characteristic of MASH.
“Hepatocyte apoptosis is a key feature of metabolic dysfunction–associated steatohepatitis (MASH)”
From Impaired TIM4-mediated efferocytosis by liver macrophages contributes to fibrosis in metabolic dysfunction–associated steatohepatitis (2025) · cites this paper as [6]
In NASH, hepatocytes undergo apoptosis, necroptosis or pyroptosis, thereby initiating inflammation.
“In NASH, hepatocytes undergo apoptosis, necroptosis or pyroptosis (a newly described caspase 1-dependent apoptosis observed in NASH),33 thereby initiating inflammation in several ways.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [33]
Efferocytosis of apoptotic hepatocytes by phagocytes triggers macrophages to release TGFβ.
“Whilst this process has anti-inflammatory potential, as it removes intracellular content which could otherwise act as DAMPs, efferocytosis also triggers macrophages to release transforming growth factor (TGF)β.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [33]

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“Necroptosis is probably the best-understood form of regulated necrosis, since it shares multiple molecular components with the extrinsic apoptotic pathway and can act as a fail-safe mechanism to ensure cell death progression when apoptosis is abnormally inhibited, which may also be relevant in pathological conditions…”
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FGF21: An Emerging Therapeutic Target for Non-Alcoholic Steatohepatitis and Related Metabolic Diseases
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Monocyte-derived macrophages orchestrate multiple cell-type interactions to repair necrotic liver lesions in disease models
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REVIEWS IN BASIC AND CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Cell Death and Cell Death Responses in Liver Disease: Mechanisms and Clinical Relevance
Luedde, T., Kaplowitz, N., & Schwabe, R. F. (2014)
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Authors: Schwabe, R. F., & Luedde, T.
Affiliations: Columbia University Irving Medical Center (US)
Universitätsklinikum Aachen (DE)
Corresponding author: Schwabe, Robert F.
Luedde, Tom
ORCID: Schwabe, Robert F.
Luedde, Tom
Venue: Nature Reviews Gastroenterology & Hepatology
Publisher: Springer Science and Business Media LLC
Published: 2018-09-24
Volume: 15
Issue: 12
Pages: 738-752
ISSN: 1759-5045 (ISSN-L)
1759-5053
DOI: 10.1038/s41575-018-0065-y
PMC: PMC6490680
OpenAlex: W2890337997
Cited by: 582
References: 185
Citations by year: 2026: 51 · 2025: 82 · 2024: 93 · 2023: 91 · 2022: 94 · 2021: 78 · 2020: 59 · 2019: 33
FWCI: 4.17
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Gastroenterology & Hepatology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Alcohol Abuse and Alcoholism (U01AA021912)
National Cancer Institute (R01CA190844, R01CA200597)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK116620)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords: apoptosis, necroptosis, programmed cell death, liver injury, acute liver failure, chronic liver disease, liver fibrosis, liver cirrhosis, liver cancer, non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, hepatic stellate cells, hepatocyte turnover, cell death detection
MeSH terms: Animals, Humans, Liver, Liver Diseases, Necrosis, Cell Death, Apoptosis

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Apoptosis and necroptosis in the liver: a matter of life and death

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