Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mechanisms underlying the antifibrotic properties of noninhibitory PAI-1 (PAI-1R) in experimental nephritis.

American journal of physiology. Renal physiology - 1 Oct 2009

Huang Yufeng, Border Wayne A, Lawrence Daniel A, Noble Nancy A

Abstract excerpt

Administration of a mutant, noninhibitory PAI-1 (PAI-1R), reduces disease in experimental glomerulonephritis. Here we investigated the importance of vitronectin (Vn) binding, PAI-1 stability and protease binding in this therapeutic effect using a panel of PAI-1 mutants differing in half-life, protease binding, and Vn binding. PAI-1R binds Vn normally but does not inhibit proteases. PAI-1AK has a complete defect...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Collagen Type I
Share to Glomerulonephritis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Isoantibodies

Share to Peptide Hydrolases

Share to Plasminogen Activator Inhibitor 1

Share to Proteinuria

Share to Transforming Growth Factor beta1

Share to Vitronectin

Source

Open in PubMed Open full text

Identifiers

PMID: 19625379
DOI: 10.1152/ajprenal.00024.2009
PMCID: PMC2775568

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mechanisms underlying the antifibrotic properties of noninhibitory PAI-1 (PAI-1R) in experimental nephritis.PMID 19625379Read ↗

A mutant, noninhibitory plasminogen activator inhibitor type 1 decreases matrix accumulation in experimental glomerulonephritis.Semantic proximity Read ↗

Noninhibitory PAI-1 enhances plasmin-mediated matrix degradation both in vitro and in experimental nephritis.Semantic proximity Read ↗

Renal fibrosis: not just PAI-1 in the sky.Semantic proximity Read ↗

Structure-function relationships of plasminogen activator inhibitor-1 and its potential as a therapeutic agent.Semantic proximity Read ↗

Distal hinge of plasminogen activator inhibitor-1 involves its latency transition and specificities toward serine proteases.Semantic proximity Read ↗

The Molecular Basis for Anti-Proteolytic and Non-Proteolytic Functions of Plasminogen Activator Inhibitor Type-1: Roles of the Reactive Centre Loop, the Shutter Region, the Flexible Joint Region and the Small Serpin FragmentSemantic proximity Read ↗

Structural differences between active forms of plasminogen activator inhibitor type 1 revealed by conformationally sensitive ligands.Semantic proximity Read ↗

Mapping of binding sites for heparin, plasminogen activator inhibitor-1, and plasminogen to vitronectin's heparin-binding region reveals a novel vitronectin-dependent feedback mechanism for the control of plasmin formation.Semantic proximity Read ↗

A plasminogen activator inhibitor type 1 mutant retards diabetic nephropathy in db/db mice by protecting podocytes.Semantic proximity Read ↗

Multifunctionality of PAI-1 in fibrogenesis: evidence from obstructive nephropathy in PAI-1-overexpressing mice.Semantic proximity Read ↗

Vitronectin accumulates in the interstitium but minimally impacts fibrogenesis in experimental chronic kidney disease.Semantic proximity Read ↗

Mutants of plasminogen activator inhibitor-1 designed to inhibit neutrophil elastase and cathepsin G are more effective in vivo than their endogenous inhibitors.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.