ArticleFrontiers in immunology2022
A novel fusion protein consisting of anti-ANGPTL3 antibody and interleukin-22 ameliorates diabetic nephropathy in mice.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting ANGPTL3 and IL-33/ST2 Ameliorates Diabetic Kidney Disease by Reducing Lipotoxicity, Alleviating Inflammation and Inhibiting Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Anti-ANGPTL3 antibody and IL-22 fusion protein mitigate nephrotic syndrome via mitochondrial protection, anti-apoptosis, and autophagy suppression.Antibody therapeutics · 2026Article
- Urinary ANGPTL3: a novel noninvasive biomarker for podocyte injury in pediatric glomerular diseases.Journal of translational medicine · 2026Article
- Targeting angiopoietin-like protein 3 and interleukin-1β alleviated liver and kidney injury through attenuation of lipotoxicity and regulation of glycolipid metabolism in db/db mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Canagliflozin Attenuates Podocyte Inflammatory Injury through Suppressing the TXNIP/NLRP3 Signaling Pathway in Diabetic Kidney Disease Mice.Inflammation · 2025Article
- The significance of ANGPTL3 and ANGPTL4 proteins in the development of dyslipidemia in Type 2 diabetes mellitus.Journal of family medicine and primary care · 2025Article
- Simultaneously blocking ANGPTL3 and IL-1β for the treatment of atherosclerosis through lipid-lowering and anti-inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- IL-22 is secreted by proximal tubule cells and regulates DNA damage response and cell death in acute kidney injury.Kidney international · 2024Article
- Angiopoietin-like protein 4 dysregulation in kidney diseases: a promising biomarker and therapeutic target.Frontiers in pharmacology · 2024Review
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The pathogenic mechanisms of diabetic nephropathy (DN) include podocyte injury, inflammatory responses and metabolic disorders. Although the antagonism of Angiopoietin-like protein 3 (ANGPTL3) can alleviate proteinuria symptoms by inhibiting the activation of integrin αvβ3 on the surface of podocytes, it can not impede other pathological processes, such as inflammatory responses and metabolic dysfunction of glucolipid. Interleukin-22 (IL-22) is considered to be a pivotal molecule involved in suppressing inflammatory responses, initiating regenerative repair, and regulating glucolipid metabolism. Methods: Genes encoding the mIL22IgG2aFc and two chains of anti-ANGPTL3 antibody and bifunctional protein were synthesized. Then, the DN mice were treated with intraperitoneal injection of normal saline, anti-ANGPTL3 (20 mg/kg), mIL22Fc (12 mg/kg) or anti-ANGPTL3 /IL22 (25.3 mg/kg) and irrigation of positive drug losartan (20mg/kg/d) twice a week for 8 weeks. Results: In this research, a novel bifunctional fusion protein (anti-ANGPTL3/IL22) formed by the fusion of IL-22 with the C-terminus of anti-ANGPTL3 antibody exhibited favorable stability and maintained the biological activity of anti-ANGPTL3 and IL-22, respectively. The fusion protein showed a more pronounced attenuation of proteinuria and improved dysfunction of glucolipid metabolism compared with mIL22Fc or anti-ANGPTL3. Our results also indicated that anti-ANGPTL3/IL22 intervention significantly alleviated renal fibrosis Conclusion: Collectively, anti-ANGPTL3/IL22 bifunctional fusion protein can be a promising novel therapeutic strategy for DN by reducing podocyte injury, ameliorating inflammatory response, and enhancing renal tissue recovery.
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