ArticleMolecular medicine (Cambridge, Mass.)2023
PINK1 protects against dendritic cell dysfunction during sepsis through the regulation of mitochondrial quality control.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- New trends and hotspots in sepsis-related protein post-translational modification: a bibliometric and visual analysis.Frontiers in medicine · 2025Pooled it
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- PINK1-Parkin pathway-mediated mitophagy in sepsis: friend or foe?Molecular biology reports · 2026Review
- Mitophagy-driven multidimensional regulation of tumor immune evasion and context-dependent therapeutic strategies.Journal of translational medicine · 2026Review
- The Neuroimmune Axis in Sepsis: From Pathophysiological Circuits to Precision Neuromodulation.Journal of inflammation research · 2026Review
- Investigating the Mechanisms of Mitochondrial Dysfunction in Ischemic Stroke and Predicting Therapeutics Through Machine Learning and Integrated Bioinformatics.Current medicinal chemistry · 2026Article
- Dendritic-cell depletion and dysfunction in sepsis: a compartment- and evidence-aware synthesis.Frontiers in immunology · 2026Review
- Systems-level analysis uncovers eight hub genes and a resveratrol-based therapeutic strategy for ischemic stroke.Frontiers in pharmacology · 2026Article
- From powerhouse to modulator: regulating immune system responses through intracellular mitochondrial transfer.Cell communication and signaling : CCS · 2025Review
- Mediating role of blood metabolites in the relationship between immune cell traits and sepsis: a Mendelian randomization and mediation analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Nuclear fragile X mental retardation-interacting protein 1-mediated ribophagy regulates immune function of dendritic cells in polymicrobial sepsis.Burns & trauma · 2025Article
- Dysregulated dendritic cells in sepsis: functional impairment and regulated cell death.Cellular & molecular biology letters · 2024Review
- Mechanism and role of mitophagy in the development of severe infection.Cell death discovery · 2024Review
- Restoring the infected powerhouse: Mitochondrial quality control in sepsis.Redox biology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDendritic cell (DC) dysfunction plays a central role in sepsis-induced immunosuppression. Recent research has indicated that collective mitochondrial fragmentation contributes to the dysfunction of immune cells observed during sepsis. PTEN-induced putative kinase 1 (PINK1) has been characterized as a guide for impaired mitochondria that can keep mitochondrial homeostasis. However, its role in the function of DCs during sepsis and the related mechanisms remain obscure. In our study, we elucidated the effect of PINK1 on DC function during sepsis and its underlying mechanism of action.
methodsCecal ligation and puncture (CLP) surgery and lipopolysaccharide (LPS) treatment were used as in vivo and in vitro sepsis models, respectively.
resultsWe found that changes in mitochondrial PINK1 expression of DCs paralleled changes in DC function during sepsis. The ratio of DCs expressing MHC-II, CD86, and CD80, the mRNAs level of dendritic cells expressing TNF-α and IL-12, and the level of DC-mediated T-cell proliferation were all decreased, both in vivo and in vitro during sepsis, when PINK1 was knocked out. This suggested that PINK1 knockout prevented the function of DCs during sepsis. Furthermore, PINK1 knockout inhibited Parkin RBR E3 ubiquitin protein (Parkin)-dependent mitophagy and enhanced dynamin-related protein 1 (Drp1)-related mitochondrial fission, and the negative effects of PINK1 knockout on DC function following LPS treatment were reversed by Parkin activation and Drp1 inhibitor. Knockout of PINK1 also increased apoptosis of DCs and the mortality of CLP mice.
conclusionOur results indicated that PINK1 protected against DC dysfunction during sepsis through the regulation of mitochondrial quality control.
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