The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.
Danger-Associated Molecular Patterns (DAMPs): Molecular Triggers for Sterile Inflammation in the Liver
Open accessAbstract
Inflammatory liver diseases in the absence of pathogens such as intoxication by xenobiotics, cholestatic liver injury, hepatic ischemia-reperfusion injury (I/R), non-alcoholic steatohepatitis (NASH), or alcoholic liver disease (ALD) remain threatening conditions demanding specific therapeutic options. Caused by various different noxae, all these conditions have been recognized to be triggered by danger- or death-associated molecular patterns (DAMPs), discompartmentalized self-structures released by dying cells. These endogenous, ectopic molecules comprise proteins, nucleic acids, adenosine triphosphate (ATP), or mitochondrial compounds, among others. This review resumes the respective modes of their release—passively by necrotic hepatocytes or actively by viable or apoptotic parenchymal cells—and their particular roles in sterile liver pathology. It addresses their sensors and the initial inflammatory responses they provoke. It further addresses a resulting second wave of parenchymal death that might be of different mode, boosting the release of additional, second-line DAMPs. Thus, triggering a more complex and pronounced response. Initial and secondary inflammatory responses comprise the activation of Kupffer cells (KCs), the attraction and activation of monocytes and neutrophil granulocytes, and the induction of type I interferons (IFNs) and their effectors. A thorough understanding of pathophysiology is a prerequisite for identifying rational therapeutic targets.
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“Damage-associated molecular patterns (DAMPs), like high-mobility group box 1 (HMGB1) or fragmented DNA, are released from hepatocytes. Endogenous danger stimuli bind to Toll-like receptor 4(TRL4) with the MyD88 adaptor protein in Kupffer cells. TLR4/MyD88, prompts the protein NF-κB to lead to the generation of pro-inflammatory and pro-fibrotic mediators associated with the disease—such as TGF-β1”
From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [33]
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In the citing paper
“Pro-inflammatory cytokines TNF-α and IL-1β (secreted by M1 macrophages) activate NF-κB within HSCs, inducing pro-fibrotic gene expression and inhibiting HSC apoptosis.”
From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [33]
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In the citing paper
“TGF-β1 (released by Kupffer cells, platelets, and injured hepatocytes) binds to TβRII receptors on HSCs, leading to phosphorylation of Smad2/3. The phospho-Smad2/3-Smad4 complex translocates to the nucleus, activating genes encoding α-smooth muscle actin (α-SMA), collagen I and III, and tissue inhibitor of metalloproteinase-1 (TIMP-1) while suppressing matrix metalloproteinases (MMPs).”
From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [33]
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“Chemokines such as CCL2 and CXCL8 recruit monocytes, perpetuating the inflammatory response and fibrosis [33, 34].”
From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [33]
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Metadata
- Authors
- Mihm, S.
- Affiliations
- Universitätsmedizin Göttingen (DE)
- Corresponding author
- Mihm, Sabine
- ORCID
- Mihm, Sabine
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2018-10-10
- Volume
- 19
- Issue
- 10
- Pages
- 3104
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC6213769
- OpenAlex
- W2896394478
- Cited by
- 232
- References
- 123
- Citations by year
- 2026: 27 · 2025: 30 · 2024: 32 · 2023: 35 · 2022: 34 · 2021: 25 · 2020: 32 · 2019: 16 · 2018: 1
- FWCI
- 1.87
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- damage-associated molecular patterns, sterile inflammation, liver inflammation, liver necrosis, apoptosis, Kupffer cells, monocytes, neutrophils, type I interferon, nonalcoholic steatohepatitis, alcoholic liver disease, cholestatic liver injury, hepatic ischemia-reperfusion injury, innate immune recognition
- MeSH terms
- Alarmins, Pathogen-Associated Molecular Pattern Molecules, Adenosine Triphosphate, Animals, Hepatitis, Humans, Keratins, Mitochondria, Liver, Biomarkers, HMGB1 Protein
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