ArticleFrontiers in immunology2023
The landscape of mitophagy in sepsis reveals PHB1 as an NLRP3 inflammasome inhibitor.
Article in Frontiers in immunology, 2023. 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, 21 citations in OpenAlex.
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- Single-cell mitophagy signature-based artificial intelligence model enhances prediction of prognosis and immunotherapy response in non-small-cell lung cancer.Respiratory research · 2026Article
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Targeted autophagy: research progress on the regulatory potential of periodontitis prevention and treatment.Frontiers in cell and developmental biology · 2026Review
- The central role of mitochondrial pathology in sepsis-induced cardiomyopathy: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- Prohibitins: emerging host targets of bacteria and viruses at the plasma membrane, mitochondria, and cytoplasm.Microbial cell (Graz, Austria) · 2026Article
- Bidirectional Regulation of NLRP3 Inflammasome and Mitochondrial Quality Control in Sepsis: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- PHB1 Attenuates Triptolide-induced Cardiotoxicity by Regulating Mitochondrial Dynamics in Cultured Newborn Mice Cardiomyocytes.Journal of cardiovascular pharmacology · 2026Article
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- Development of a Piezoelectric Immunosensor to Rapidly Measure Prohibitin‑1 as a Prognostic Biomarker for Sepsis and Other Serious Infectious Diseases.ACS applied electronic materials · 2025Article
- DIRAS1 Drives Oxaliplatin Resistance in Colorectal Cancer via PHB1-Mediated Mitochondrial Homeostasis.Biology · 2025Article
- Reassessing sepsis research: new clues for old players and new players for an old symptom to improve patient outcomes.EXCLI journal · 2025Review
- Flufenamic acid inhibits pyroptosis in ischemic flaps via the AMPK-TRPML1-Calcineurin signaling pathway.Burns & trauma · 2025Article
- Targeting selective autophagy and beyond: From underlying mechanisms to potential therapies.Journal of advanced research · 2024Review
- Article
- Mechanism and role of mitophagy in the development of severe infection.Cell death discovery · 2024Review
- Molecular mechanisms of Sepsis attacking the immune system and solid organs.Frontiers in medicine · 2024Review
- Restoring the infected powerhouse: Mitochondrial quality control in sepsis.Redox biology · 2023Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitophagy is a selective autophagy targeting damaged and potential cytotoxic mitochondria, which can effectively prevent excessive cytotoxic production from damaged mitochondria and alleviate the inflammatory response. However, the potential role of mitophagy in sepsis remains poorly explored. Here, we studied the role of mitophagy in sepsis and its immune heterogeneity. By performing mitophagy-related typing on 348 sepsis samples, three clusters (A, B, and C) were obtained. Cluster A had the highest degree of mitophagy accompanied by lowest disease severity, while cluster C had the lowest degree of mitophagy with the highest disease severity. The three clusters had unique immune characteristics. We further revealed that the expression of PHB1 in these three clusters was significantly different and negatively correlated with the severity of sepsis, suggesting that PHB1 was involved in the development of sepsis. It has been reported that impaired mitophagy leads to the over-activation of inflammasomes, which promotes sepsis development. Further analysis showed that the expressions of NLRP3 inflammasomes core genes in cluster C were significantly up-regulated and negatively correlated with PHB1. Next, we verified whether PHB1 downregulation caused the activation of inflammasomes and found that the PHB1 knockdown increased the levels of mtDNA in the cytoplasm and enhanced the activation of NLRP3 inflammasomes. In addition, mitophagy inhibitor treatment abolished PHB1 knockdown-mediated activation of NLRP3 inflammasomes, suggesting that PHB1 inhibited the activation of inflammasomes through mitophagy. In conclusion, this study reveals that a high degree of mitophagy may predict a good outcome of sepsis, and PHB1 is a key NLRP3 inflammasome regulator
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