Evidence map›Paper›PMID 26290372›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Human anti-α3(IV)NC1 antibody drug conjugates target glomeruli to resolve nephritis.

Nino Kvirkvelia, Malgorzata McMenamin, Vanessa Iris Gutierrez, Besarion Lasareishvili, Michael P Madaio

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Targeted therapeutic strategies for the kidney.Expert opinion on therapeutic targets · 2024
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Novel Drug Delivery Technologies and Targets for Renal Disease.Hypertension (Dallas, Tex. : 1979) · 2022
    Review
  8. Targeted Drug Delivery Systems for Kidney Diseases.Frontiers in bioengineering and biotechnology · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Targeting cytokine signaling in salt-sensitive hypertension.American journal of physiology. Renal physiology · 2016
    Review
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

5 authors at 2 institutions in 2 countries.

Nino KvirkveliaDepartment of Medicine, Georgia Regents University, Augusta, Georgia; and.ORCID http://orcid.org/0000-0001-7068-1612
Malgorzata McMenaminDepartment of Medicine, Georgia Regents University, Augusta, Georgia; and.
Vanessa Iris GutierrezDepartment of Medicine, Georgia Regents University, Augusta, Georgia; and.
Besarion LasareishviliAgricultural University of Georgia, Tbilisi, Georgia.
Michael P MadaioDepartment of Medicine, Georgia Regents University, Augusta, Georgia; and mmadaio@gru.edu.
Augusta University · USAgricultural University of Georgia · GE

Funding

Novel peptide-based strategy to inhibit deleterious TNF signaling in nephrotoxic nephritisR01DK100564 · NIDDK · AUGUSTA UNIVERSITY · PI LUCAS, RUDOLF, MADAIO, MICHAEL P · 2015 to 2017
$684k
NIDDK NIH HHS DK0811140NIDDK NIH HHS R01 DK100564
6 · The paper itself

Abstract

Current therapies to limit kidney disease progression lack specificity and often have systemic toxicity. To approach this problem, we postulated that a human monoclonal antibody (F1.1), directed against the noncollagenous-1 domain (NC1) of α3(IV) collagen that localizes in glomeruli, could serve as a vehicle for targeted drug delivery. Given enhanced exposure of the NC1 domain of α3(IV) during glomerular diseases, with limited epitope expression in other organs, α3(IV)NC1 provides an ideal target for delivery of disease-modifying agents. As a potential disease-modifying agent, we initially took advantage of recent observations that PGE2 promoted recovery after established injury during the course of nephrotoxic nephritis. To address the general applicability of the approach, the efficacy of glomerular delivery of dexamethasone was also examined. To achieve glomerular targeted therapy, PGE2 and dexamethasone were coupled to F1.1. After confirmation of the composition and activity of the conjugates, both glomerular localization and the capacity of the conjugates to modify disease were evaluated. After injection into mice with established nephritis, resolution of disease was enhanced with both agents, with normalization of histology and improved blood urea nitrogen levels in conjugate-treated mice compared with untreated mice. The results provide a novel means of targeting glomeruli during nephritis, irrespective of cause, by providing efficient drug delivery, with the potential of limiting systemic effects.

Indexed as

AnimalsAntibodies, MonoclonalAnti-Glomerular Basement Membrane DiseaseAnti-Inflammatory AgentsAutoantigensBlood Urea NitrogenCell LineCollagen Type IVDexamethasoneDinoprostoneDrug Delivery SystemsFemaleHepatocytesHumansImmunoconjugatesKidney GlomerulusAntibodies, MonoclonalAnti-Inflammatory AgentsAutoantigensCollagen Type IVDexamethasoneDinoprostoneImmunoconjugatestype IV collagen alpha3 chainantibody-drug conjugatesglomerulinephritistargeted delivery

Identifiers

PMID26290372
PMCPMC4609920
OpenAlexW2181498209

What OpenQuestion holds

Textmetadata
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.