ArticleCell death discovery2024
Blocking CIRP protects against acute pancreatitis by improving mitochondrial function and suppressing pyroptosis in acinar cells.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Beyond Supportive Care: Mitochondria as a Strategic Therapeutic Avenue in Acute Pancreatitis.Digestive diseases and sciences · 2026Review
- Heparin inhibits NLRP3-dependent pyroptosis in acute pancreatitis.Genes and immunity · 2026Article
- Induction of stress granules alleviates programmed cell death induced by lysosomal damage during NK cell cryopreservation.Cell death discovery · 2026Article
- Macrophage TRIM21 Inhibition Ameliorates Murine Acute Pancreatitis via PHB2-Mediated Mitochondrial Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Cold-Inducible RNA-Binding Protein Attenuates Pancreatic Fibrosis by Suppressing Pyroptosis in Chronic Pancreatitis.Inflammation · 2026Article
- Cold exposure increases aortic dissection risk through extracellular cold inducible RNA binding protein and toll like receptor 4 signaling.Scientific reports · 2026Article
- Inhibition of PTP1B Through NADH Dehydrogenase Activity Reduces Acute Pancreatic Acinar Cell Pyroptosis by Inhibiting the ROS/TXNIP/NLRP3 Pathway.Digestive diseases and sciences · 2026Article
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- The Role of Cold-Inducible RNA-Binding Protein (CIRP) in Neurological Disorders.Brain sciences · 2026Review
- Tangled contacts: mitochondrial interactions with cellular organelles in acute pancreatitis.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
- Nanotherapy for Pancreatitis: From Single-Cell Targeting Toward Multicellular-Coordinated Regulation.International journal of nanomedicine · 2026Review
- Translational Pharmaco-Nutritional Approaches in the Management of Clinical Acute Pancreatitis-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Naa10p impairs PGC-1α/Pparγ2 interaction to inhibit mitochondrial protection in pancreatitis.Journal of cell communication and signaling · 2025Article
- Therapeutic potential of plant polyphenols in acute pancreatitis.Inflammopharmacology · 2025Review
- Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches.Journal of neuroinflammation · 2025Review
- Anti-DAMP therapies for acute inflammation.Frontiers in immunology · 2025Review
- Pancreatic stone protein inhibits pyroptosis of pancreatic acinar cells in sepsis-associated pancreatic injury.Frontiers in medicine · 2025Article
- Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Acute pancreatitis (AP) continues to pose a major challenge as targeted therapeutic interventions are absent. Mitochondrial dysfunction and inflammasome-dependent pyroptosis are involved in the pathogenic mechanisms of AP. CIRP is a stress-response protein and a damage-associated molecular pattern (DAMP) molecule. In our previous studies, we discovered that excessive CIRP can directly damage pancreatic acinar cells. Nonetheless, the precise involvement of CIRP in AP is still unexplored. The primary aim of this study was to examine the potential involvement of CIRP in the development of pyroptosis and mitochondrial dysfunction in AP. To study this, an L-arginine-induced AP mouse model was used. Our results showed that Caspase-1-mediated pyroptosis and mitochondria-derived reactive oxygen species (ROS) were crucial factors in the occurrence of tissue damage and inflammation in AP. A substantial increase in the CIRP serum levels was observed in AP mice. Blocking CIRP by either CIRP gene knockout or systemic administration of C23, a competing inhibitor of CIRP, reduced ROS accumulation and pyroptosis in AP mice. These effects were associated with attenuated pancreatic injury and inflammation. In addition, CIRP-triggered mitochondrial dysfunction, autophagy impairment, and pyroptosis in pancreatic acinar cells were prevented by TAK242, an inhibitor of CIRP receptor TLR4. In conclusion, CIRP can induce mitochondrial dysfunction and pyroptosis in pancreatic acinar cells, and blocking CIRP may be a valuable approach to treating patients with AP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.