Evidence map›Paper›PMID 36229446›Full record

ArticleCell death & disease2022

Anti-ANGPTL3-FLD monoclonal antibody treatment ameliorates podocyte lesions through attenuating mitochondrial damage.

Qianying Lv, Xinli Han, Jiajia Ni, Qianqian Ma, Rufeng Dai, Jiaojiao Liu, Jialu Liu, Yihui Zhai, Qian Shen, Li Sun and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 3 countries.

Qianying Lv *Department of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Xinli Han *Department of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Jiajia Ni *Department of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Qianqian MaDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Rufeng DaiDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Jiaojiao LiuDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Jialu LiuDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Yihui ZhaiDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Qian ShenDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China.
Li SunShanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China.
Haimei LiuShanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China. liu__hm@163.com.
Jia RaoDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China. jiarao@fudan.edu.cn.ORCID 0000-0003-2839-3419
Hong XuDepartment of Nephrology, Children's Hospital of Fudan University, National Pediatric Medical Center of CHINA, Shanghai, China. hxu@shmu.edu.cn.
Children's Hospital of Fudan University · CNKidney Associates · USKidney Research UK · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteinuria, an indication of kidney disease, is caused by the malfunction of podocytes, which play a key role in maintaining glomerular filtration. Angiopoietin-like 3 (ANGPTL3) has been documented to have a cell-autonomous involvement in podocytes, and deletion of Angptl3 in podocytes reduced proteinuria in adriamycin-induced nephropathy. Here, we developed a monoclonal antibody (mAb) against ANGPTL3 to investigate its effects on podocyte injury in an ADR nephropathy mouse model and puromycin (PAN) induced podocyte damage in vitro. The mAb against the human ANGPTL3-FLD sequence (5E5F6) inhibited the binding of ANGPTL3-FLD to integrin β3. Treatment with the 5E5F6 mAb in ADR nephropathy mice mitigated proteinuria and led to a significant decline in podocyte apoptosis, reactive oxygen species (ROS) generation and mitochondrial fragmentation. In PAN-induced podocyte damage in vitro, the 5E5F6 mAb blocked the ANPGPLT3-mediated activation of integrin αvβ3 and Rac1, which regulated the mitochondrial homeostasis. Altogether, anti-ANGPLT3-FLD mAb attenuates proteinuria and podocyte lesions in ADR mice models, as well as PAN-induced podocyte damage, in part through regulating mitochondrial functions. Our study provides a therapeutic approach for targeting ANGPTL3 in proteinuric kidney disease.

Indexed as

Kidney DiseasesPodocytesAngiopoietin-Like Protein 3Angiopoietin-like ProteinsAngiopoietinsAnimalsAntibodies, MonoclonalDoxorubicinHumansIntegrin alphaVbeta3Integrin beta3MiceProteinuriaPuromycinReactive Oxygen SpeciesAngiopoietin-Like Protein 3Angiopoietin-like ProteinsAngiopoietinsANGPTL3 protein, humanAntibodies, MonoclonalDoxorubicinIntegrin alphaVbeta3Integrin beta3PuromycinReactive Oxygen Species

Identifiers

PMID36229446
PMCPMC9562403
OpenAlexW4304890654

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.