ArticleMolecular immunology2021
Enhanced RIPK3 kinase activity-dependent lytic cell death in M1 but not M2 macrophages.
Article in Molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Monosodium urate crystals induce lytic macrophage death partially dependent on both pyroptosis and necroptosis.Clinical rheumatology · 2026Article
- A Non-Canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver.Aging cell · 2026Article
- Targeting phenol-soluble modulin α3-driven M1 macrophage polarization and necroptosis mitigates MRSA infection in mice.Nature communications · 2026Article
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- Targeting necroptosis in Alzheimer's disease: can exercise modulate neuronal death?Frontiers in aging neuroscience · 2025Review
- Acute lung injury: a view from the perspective of necroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Diesel exhaust particles induce polarization state-dependent functional and transcriptional changes in human monocyte-derived macrophages.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Article
- The dance of macrophage death: the interplay between the inevitable and the microenvironment.Frontiers in immunology · 2024Review
- Necroptosis of macrophage is a key pathological feature in biliary atresia via GDCA/S1PR2/ZBP1/p-MLKL axis.Cell death & disease · 2023Article
- Pyroptosis, apoptosis, and autophagy are involved in infection induced by two clinicalFrontiers in cellular and infection microbiology · 2023Article
- Intracellular behavior ofFrontiers in cellular and infection microbiology · 2023Article
- Necroptosis and Alzheimer's Disease: Pathogenic Mechanisms and Therapeutic Opportunities.Journal of Alzheimer's disease : JAD · 2023Review
- Programmed cell death and lipid metabolism of macrophages in NAFLD.Frontiers in immunology · 2023Review
- ZBP1: A Powerful Innate Immune Sensor and Double-Edged Sword in Host Immunity.International journal of molecular sciences · 2022Review
- Interferon-γ Preferentially Promotes Necroptosis of Lung Epithelial Cells by Upregulating MLKL.Cells · 2022Article
- Inducible general knockout of Runx3 profoundly reduces pulmonary cytotoxic CD8Frontiers in immunology · 2022Article
- Necroptosis Contributes to Persistent Inflammation During Acute Leptospirosis.Frontiers in immunology · 2022Article
- M1 Macrophages Are More Susceptible to Necroptosis.Journal of cellular immunology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages play a crucial role in host innate immune defense against infection and tissue injury. Macrophages are highly plastic cells and their subtypes have been characterized as M1 (also termed classically activated) and M2 (alternatively activated). Although the M1/M2 paradigm has been well documented, less is known regarding the role of macrophage activation/polarization in inflammation-associated necrotic cell death. To address this gap in current knowledge, we prepared bone marrow-derived macrophages, induced them to M1 or M2 subtypes, and then investigated the expression of necroptosis signaling molecules and macrophage subtype-dependent responses to different necroptosis inducers. We found that necroptosis effector mixed lineage kinase domain-like protein (MLKL) and the key necroptosis regulator Z-DNA/RNA binding protein 1 were predominantly induced in M1 but not M2 macrophages. Interestingly, the protein but not mRNA levels of receptor-interacting protein kinase-3 (RIPK3) were also upregulated in M1 macrophages. We further found that macrophage necrotic cell death, the releases of lactate dehydrogenase and dead cell proteases as well as MLKL phosphorylation at Ser345 in response to various necroptosis inducers were greatly augmented in M1 but not M2 macrophages, and the accelerated effects were blocked by two structurally distinct specific RIPK3 inhibitors GSK872 or GSK843. Thus, our findings demonstrate that M1 but not M2 subtypes of macrophages are more susceptible to inflammation-related lytic cell death in an RIPK3 kinase activity-dependent manner.
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Registered trials
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