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Updated: May 12, 2026
Reliable and High Efficiency Extraction of Kidney Immune Cells
Published on: August 19, 2016
Depleting profibrotic macrophages using bioactivated in vivo assembly peptides ameliorates kidney fibrosis
Qing Ouyang1, Chao Wang2,3, Tian Sang2
1Department of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, 100853, China. nolimithyer3169@outlook.com.
Abstract:
Managing renal fibrosis is challenging owing to the complex cell signaling redundancy in diseased kidneys. Renal fibrosis involves an immune response dominated by macrophages, which activates myofibroblasts in fibrotic niches. However, macrophages exhibit high heterogeneity, hindering their potential as therapeutic cell targets. Herein, we aimed to eliminate specific macrophage subsets that drive the profibrotic immune response in the kidney both temporally and spatially. We identified the major profibrotic macrophage subset (Fn1+Spp1+Arg1+) in the kidney and then constructed a 12-mer glycopeptide that was designated as bioactivated in vivo assembly PK (BIVA-PK) to deplete these cells. BIVA-PK specifically binds to and is internalized by profibrotic macrophages. By inducing macrophage cell death, BIVA-PK reshaped the renal microenvironment and suppressed profibrotic immune responses. The robust efficacy of BIVA-PK in ameliorating renal fibrosis and preserving kidney function highlights the value of targeting macrophage subsets as a potential therapy for patients with CKD.
Insights
Targeting specific kidney macrophages with a novel glycopeptide (BIVA-PK) effectively reduced renal fibrosis. This approach suppressed profibrotic immune responses, offering a promising new therapy for chronic kidney disease (CKD).
Area of Science:
- Immunology
- Nephrology
- Molecular Biology
Background:
- Renal fibrosis management is complex due to intricate kidney cell signaling.
- Macrophages drive the immune response in renal fibrosis, activating myofibroblasts.
- Macrophage heterogeneity complicates their use as therapeutic targets.
Purpose of the Study:
- To eliminate specific kidney macrophage subsets driving profibrotic immune responses.
- To develop a targeted therapy for renal fibrosis.
- To investigate the therapeutic potential of depleting profibrotic macrophages.
Main Methods:
- Identification of the major profibrotic macrophage subset (Fn1+Spp1+Arg1+) in the kidney.
- Construction of a 12-mer glycopeptide, bioactivated in vivo assembly PK (BIVA-PK), for targeted cell depletion.
- Administration of BIVA-PK to induce targeted macrophage cell death.
Main Results:
- BIVA-PK specifically bound to and was internalized by profibrotic macrophages.
- BIVA-PK induced targeted macrophage cell death, reshaping the renal microenvironment.
- The treatment suppressed profibrotic immune responses, ameliorating renal fibrosis and preserving kidney function.
Conclusions:
- Targeting specific profibrotic macrophage subsets is a viable therapeutic strategy for renal fibrosis.
- BIVA-PK demonstrates robust efficacy in preclinical models of kidney fibrosis.
- This approach holds promise for treating patients with chronic kidney disease (CKD).
