Targeting the recruitment of monocytes and macrophages in renal disease.
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Summary
Experimental tools to target renal macrophage recruitment by using antagonists against selectins, chemokines, integrins, or other important cytokines that mediate renal injury via macrophages are discussed, some of these already having been used in clinical trials.
- Type
- review
- Published
- 2010-05-01
- Cited by
- 72
- References
- 119
- OpenAlex
- https://openalex.org/W1994438181
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:28171763
Keywords
Macrophage, Inflammation, Proinflammatory cytokine, Fibrosis, Chemokine
References
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- Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation 1
- Intervention of crescentic glomerulonephritis by antibodies to monocyte chemotactic and activating factor (MCAF/MCP‐1)
- Chemokine Receptor CCR1 Regulates Inflammatory Cell Infiltration after Renal Ischemia-Reperfusion Injury
- Met‐RANTES reduces vascular and tubular damage during acute renal transplant rejection: blocking monocyte arrest and recruitment
- Lack of chemokine receptor CCR1 enhances Th1 responses and glomerular injury during nephrotoxic nephritis.
- The role of interstitial macrophages in nephropathy of type 2 diabetic db/db mice.
- Expression of the chemokines MCP-1/CCL2 and RANTES/CCL5 is differentially regulated by infiltrating inflammatory cells.
- Specialized roles of the chemokine receptors CCR1 and CCR5 in the recruitment of monocytes and T(H)1-like/CD45RO(+) T cells.
- P-selectin deficiency exacerbates experimental glomerulonephritis: a protective role for endothelial P-selectin in inflammation.
- Fractalkine receptor (CX3CR1) inhibition is protective against ischemic acute renal failure in mice.
- Contribution of CD11a/CD18, CD11b/CD18, ICAM‐1 (CD54) and −2 (CD102) to human monocyte migration through endothelium and connective tissue fibroblast barriers
- DNA vaccination with naked DNA encoding MCP-1 and RANTES protects against renal injury in adriamycin nephropathy.
- Prevention of crescentic glomerulonephritis by immunoneutralization of the fractalkine receptor CX3CR1 rapid communication.
- CCR1 blockade reduces interstitial inflammation and fibrosis in mice with glomerulosclerosis and nephrotic syndrome.
- Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines.
- Monitoring of Blood Vessels and Tissues by a Population of Monocytes with Patrolling Behavior
Cited by
- IL‐22 sustains epithelial integrity in progressive kidney remodeling and fibrosis
- Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways
- Mononuclear phagocyte system in kidney disease and repair
- Necroinflammation in Kidney Disease.
- Deposition of the lectin pathway of complement in renal biopsies of lupus nephritis patients.
- Four danger response programs determine glomerular and tubulointerstitial kidney pathology
- RAGE-mediated interstitial fibrosis in neonatal obstructive nephropathy is independent of NF-κB activation.
- Escherichia coli Shiga Toxin Mechanisms of Action in Renal Disease
- Macrophages and renal fibrosis.
- Effects of the mTOR inhibitor Rapamycin on Monocyte-Secreted Chemokines
- Danger Control Programs Cause Tissue Injury and Remodeling
- Cellular mechanisms of tissue fibrosis. 3. Novel mechanisms of kidney fibrosis.
- Monocytes induce proximal tubular epithelial–mesenchymal transition through NF‐kappa B dependent upregulation of ICAM‐1
- 1,25-Dihydroxyvitamin D3 Promotes High Glucose-Induced M1 Macrophage Switching to M2 via the VDR-PPARγ Signaling Pathway
- Optimal Structural Design of Mannosylated Nanocarriers for Macrophage Targeting
- AKI in the ICU: definition, epidemiology, risk stratification, and outcomes.
- Cellular and molecular mechanisms of renal fibrosis
- TREM-1 regulates macrophage polarization in ureteral obstruction.
- Immunoaffinity capillary electrophoresis: A new versatile tool for determining protein biomarkers in inflammatory processes
- Renal microenvironments and macrophage phenotypes determine progression or resolution of renal inflammation and fibrosis.
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