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Journal of Nanobiotechnology logoLink to Journal of Nanobiotechnology
. 2024 Jan 23;22:38. doi: 10.1186/s12951-023-02232-3

Correction: Microenvironment of pancreatic inflammation: calling for nanotechnology for diagnosis and treatment

Lu Liu 1,#, Yiqing Zhang 2,3,#, Xinghui Li 1,, Jun Deng 1,2,
PMCID: PMC10807150  PMID: 38263033

Correction: Journal of Nanobiotechnology (2023) 21:443 10.1186/s12951-023-02200-x

Following publication of the original article [1], the cells in Table 1 were not formatted and aligned correctly.

Table 1.

Nanotechnology-based strategies for the diagnosis and treatment of acute pancreatitis

Category Indicators Nanoagents (Size) Animal models Mechanisms Modes Refs.
Inflammatory cells Macrophage

Lip-DTPA@AuNP(17.2 ± 2.1 nm)

M-Gd-NL (120.2 ± 8.5 nm)

Caerulein and LPS-induced AP

l-Arginine-induced AP

Gd (III) contrast agents loading of AuNPs and localization to pancreatic tissue for MR imaging Diagnosis [47]

Gd-DTPA-Cy5.5-PsLmAb

(50 mm)

CO-HbV (~ 280 nm)

Caerulein-induced AP, l-A-arginine-induced AP

Targeting macrophages and increasing T1 Imaging ability Diagnosis [48]

G4.5-COOH, G5-OH (5 nm)

SPIO-clodronate-liposomes (100–200 nm)

MU (175 nm)

Caerulein-induced AP P-selectin-targeted MR/NIRF bimodal imaging improves spatial resolution and sensitivity. Diagnosis [49]

Sodium taurocholate-induced SAP

Caerulein-induced AP

Targeting macrophages and polarizing macrophages toward an M2-like phenotype Therapy [56]
Inhibition of NF-κB nuclear translocation in macrophages and a reduction in inflammatory cells Therapy [57]
Selectively inducing macrophage apoptosis and reducing the release of inflammatory mediators Diagnosis and therapy [59]
Significantly inhibiting the secretion of pro-inflammatory cytokines TNF-α and IL-6 by macrophages Therapy [60]
Neutrophil tFNAs (~ 10 nm) Sodium taurocholate-induced AP Suppressing the secretion of inflammatory cytokines and regulating the expression of specific apoptotic and anti-apoptotic proteins Therapy [67]
CQ-LPs/TAM-NPs(152.8 ± 2.26/153.2 ± 3.05 nm) Caerulein and LPS-induce SAP CQ in combination with TAM syner-gistically promoted iNOS/IDO expression Therapy [68]
NNPs/CLT (61.4 ± 2.8 nm、156.8 ± 2.3 nm、303.7 ± 1.3 nm) 3% Sodium taurocholate-induce AP Significantly downregulating the levels of serum amylase and pancreatic myeloperoxidase elevant pro-inflammatory cytokines Therapy [74]
Oxidative stress and ROS

CAPE-loaded-NL (309 ± 54 nm)

RA-EMP (4.703 ± 0.114 nm)

l-Ornithine-induced AP Modulating Nrf2 and NF-κB Signaling Therapy [83]
l-Arginine-induced AP Suppressing the effects of oxidative stress and proinflammatory cytokines Therapy [84]
NC (82 ± 5.4 nm) Caerulein-induced AP Upregulation of Nrf2, SOD1 and NQO1, downregulating the iNOS, p65-NF-κB, Hsp27 and Hsp70 Therapy [87]
NY (159 ± 7.5 nm) Caerulein-induced AP Reducing mitochondrial and ER stress via modulation of Nrf2-NFκB pathway Therapy [88]
Pbzyme (~ 110-nm) Caerulein-induced AP Inhibiting TLRs/NF-κB signaling pathways and scavenging ROS Therapy [17]

MoSe2-PVP NPs (119.39 ± 13.94 nm)

MoSe2@PVP NSs (86.278 ± 11.82 nm)

Caerulein-induced AP Mimicking CAT, SOD, POD, GPx and eliminating a variety of ROS Therapy [89]
Caerulein-induced AP Mimicking the intrinsic multi-enzyme antioxidant activities of CAT, POD, GPx and SOD to scavenge ROS and RNS Therapy [90]
Nano-Se (20–60 nm) l-Arginine-induced AP Anti-inflammatory, antioxidant and pro-apoptotic actions Therapy [91]
CA-NPs (50–90 nm) l-Arginine and gamma radiation-induced AP Down-regulating NLRP3, NF-κB and ASK1/MAPK signal pathways and reducing malondialdehyde and caspase-3 levels. Therapy [92]
Enzymes Lipase Gd-DTPA-FA (−) l-Arginine-induced AP Upon enzymatic hydrolysis by lipase, the fat-soluble Gd-DTPA-FA is converted into a water-soluble Gd-DTPA complex, resulting in the changes of the signal intensities observed with MRI in vitro Diagnosis [96]
Proteolytic enzymes BRSNPs (268.65 ± 6.5 nm) l-Arginine-induced AP Inhibiting NF-κB pathway and activating the Nrf2/HO-1 pathway Therapy [97]
LCNPs (89–127 nm) AP Extending the circulation half-life of the model peptide compound somatostatin Therapy [98]
PLA2 MΦ-NP (L&K) (~ 100 nm)

Caerulein-induced AP

Choline-deficient ethionine (CDE) diet-induced AP

Effectively inhibiting PLA2 activity and PLA2-induced pancreatic injury Therapy [99]
pH Porous COS@SiO2 nanocomposites (~ 110 nm) Caerulein and LPS-induced SAP, l-arginine-induced SAP Activating the Nrf2 signaling pathway to inhibit oxidative stress and reduce the production of NF-κB and NLRP3 and the release of inflammatory factors Therapy [105]
l-Arginine-induced AP Dramatically enhancing gene transfection efficiency showing high targeting efficiency in pancreas Therapy [106]

Ca-CQ-pDNA-PLGA-NPs (~ 100 nm)

FA-SF-NPs (186 nm)

Biliopancreatic duct ligation- induced AP Suppressing the inflammation and oxidative stress Therapy [107]
Multi-targeting TMSN@PM (~ 142 nm) l-Arginine-induced AP Scavenging the excess ROS, degrading, and releasing manganese ions for enhanced magnetic resonance imaging Diagnosis and therapy [13]

The correct Table 1 is included in this Correction, and the original article has been corrected.

Footnotes

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Lu Liu and Yiqing Zhang have contributed equally to this work.

Contributor Information

Xinghui Li, Email: lixinghui1005@126.com.

Jun Deng, Email: djun.123@163.com.

Reference

  • 1.Liu L, Zhang Y, Li X, Deng J. Microenvironment of pancreatic inflammation: calling for nanotechnology for diagnosis and treatment. J Nanobiotechnology. 2023;21:44. doi: 10.1186/s12951-023-02200-x. [DOI] [PMC free article] [PubMed] [Google Scholar]

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