Mitochondria‐Regulated Information Processing Nanosystem Promoting Immune Cell Communication for Liver Fibrosis Regression
Open accessAbstract
Liver fibrosis is a coordinated response to tissue injury that is mediated by immune cell interactions. A mitochondria‐regulated information‐processing (MIP) nanosystem that promotes immune cell communication and interactions to inhibit liver fibrosis is designed. The MIP nanosystem mimics the alkaline amino acid domain of mitochondrial precursor proteins, providing precise targeting of the mitochondria. The MIP nanosystem is driven by light to modulate the mitochondria of hepatic stellate cells, resulting in the release of mitochondrial DNA into the fibrotic microenvironment, as detected by macrophages. By activating the STING signaling pathway, the developed nanosystem‐induced macrophage phenotype switches to a reparative subtype (Ly6C low) and downstream immunostimulatory transcriptional activity, fully restoring the fibrotic liver to its normal tissue state. The MIP nanosystem serves as an advanced information transfer system, allowing precise regulation of trained immunity, and offers a promising approach for effective liver fibrosis immunotherapy with the potential for clinical translation.
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This mitochondria-mediated HSC-macrophage crosstalk ultimately facilitated fibrosis reversal and restoration of hepatic homeostasis.
“This mitochondria-mediated HSC–macrophage crosstalk ultimately facilitated fibrosis reversal and restoration of hepatic homeostasis.”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [27]
Upon light activation, localized mitochondrial stress induced outer membrane permeabilization and release of mtDNA into the fibrotic microenvironment.
“Upon light activation, localized mitochondrial stress induced outer membrane permeabilization and release of mtDNA into the fibrotic microenvironment.”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [27]
This mtDNA was sensed by macrophages via the cGAS-STING pathway, triggering immune-stimulatory transcriptional programs and promoting their conversion toward a restorative phenotype.
“This mtDNA was sensed by macrophages via the cGAS–STING pathway, triggering immune-stimulatory transcriptional programs and promoting their conversion toward a restorative phenotype.”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [27]
Mitochondrial dysfunction and release of mitochondrial DNA act as potent danger signals in the fibrotic liver.
“Given the high mitochondrial content of hepatocytes, mitochondrial dysfunction and the release of mitochondrial DNA (mtDNA) act as potent danger signals in the fibrotic liver (27).”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [27]
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Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages
Aquino, J. B. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1792423 · Cited by 1 · see citing works
- Authors
- Che, T., Yang, X., Zhang, Y., Zheng, Y., Zhang, Y., Zhang, X., & Wu, Z.
- Affiliations
- Tianjin Medical University (CN)
- Nankai University (CN)
- Key Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging Ministry of Education; Department of Endocrinology Shandong Provincial Hospital Affiliated to Shandong First Medical University Jinan Shandong 250021 China
- Shandong Provincial Hospital (CN)
- Corresponding author
- Zhang, Xinge
- Wu, Zhongming
- Venue
- Small
- Publisher
- Wiley
- Published
- 2024-05-09
- Volume
- 20
- Issue
- 36
- Pages
- e2400413-e2400413
- ISSN
- 1613-6810 (ISSN-L)
- 1613-6829
- OpenAlex
- W4396772065
- Cited by
- 8
- References
- 7
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 3
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Small (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (32171339,82370844)
- Natural Science Foundation of Shandong Province (ZR2023MH007)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Physical Sciences › Engineering › Biomedical Engineering › Nanoplatforms for cancer theranostics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Keywords
- liver fibrosis, immune cell communication, hepatic stellate cells, mitochondrial DNA release, STING signaling, macrophage polarization, trained immunity, immunotherapy, mitochondrial precursor proteins
- MeSH terms
- Animals, Cell Communication, DNA, Mitochondrial, Humans, Liver Cirrhosis, Macrophages, Mice, Inbred C57BL, Mitochondria, Signal Transduction, Mice, Nanoparticles, Hepatic Stellate Cells
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