Evidence map›Paper›PMID 25408545›Full record

ArticleThe Journal of pathology2015

BDNF repairs podocyte damage by microRNA-mediated increase of actin polymerization.

Min Li, Silvia Armelloni, Cristina Zennaro, Changli Wei, Alessandro Corbelli, Masami Ikehata, Silvia Berra, Laura Giardino, Deborah Mattinzoli, Shojiro Watanabe and 5 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 62 citations in OpenAlex.

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  20. Role of actin cytoskeleton in podocytes.Pediatric nephrology (Berlin, Germany) · 2021
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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

15 authors at 4 institutions in 2 countries.

Min LiRenal Research Laboratory, Fondazione D'Amico per la Ricerca sulle Malattie Renali & Fondazione IRCCS Ca', Granda Ospedale Maggiore Policlinico, Milano, Italy.
Silvia Armelloni
Cristina Zennaro
Changli Wei
Alessandro Corbelli
Masami Ikehata
Silvia Berra
Laura Giardino
Deborah Mattinzoli
Shojiro Watanabe
Carlo Agostoni
Alberto Edefonti
Jochen Reiser
Piergiorgio Messa
Maria Pia Rastaldi
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITRush University Medical Center · USUniversity of Milan · ITUniversity of Trieste · IT

Funding

Proteolytic Regulation of Podocyte Function by Cathepsin L.R01DK073495 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI REISER, JOCHEN · 2006 to 2015
$2.4M
Glomerular Disease Mechanisms mediated by Podocyte TRPC6R01DK089394 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI REISER, JOCHEN · 2010 to 2014
$1.6M
NIDDK NIH HHS DK073495NIDDK NIH HHS DK089394NIDDK NIH HHS R01 DK073495NIDDK NIH HHS R01 DK089394
6 · The paper itself

Abstract

Idiopathic focal segmental glomerulosclerosis (FSGS) is a progressive and proteinuric kidney disease that starts with podocyte injury. Podocytes cover the external side of the glomerular capillary by a complex web of primary and secondary ramifications. Similar to dendritic spines of neuronal cells, podocyte processes rely on a dynamic actin-based cytoskeletal architecture to maintain shape and function. Brain-derived neurotrophic factor (BDNF) is a pleiotropic neurotrophin that binds to the tropomyosin-related kinase B receptor (TrkB) and has crucial roles in neuron maturation, survival, and activity. In neuronal cultures, exogenously added BDNF increases the number and size of dendritic spines. In animal models, BDNF administration is beneficial in both central and peripheral nervous system disorders. Here we show that BDNF has a TrkB-dependent trophic activity on podocyte cell processes; by affecting microRNA-134 and microRNA-132 signalling, BDNF up-regulates Limk1 translation and phosphorylation, and increases cofilin phosphorylation, which results in actin polymerization. Importantly, BDNF effectively repairs podocyte damage in vitro, and contrasts proteinuria and glomerular lesions in in vivo models of FSGS, opening a potential new perspective to the treatment of podocyte disorders.

Indexed as

3T3 CellsActin CytoskeletonActin Depolymerizing FactorsActinsAnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalGene Expression RegulationGlomerulosclerosis, Focal SegmentalLarvaLim KinasesMaleMiceMice, Inbred BALB CMicroRNAsPhosphorylationActin Depolymerizing FactorsActinsBDNF protein, humanBrain-Derived Neurotrophic FactorLim KinasesMicroRNAsMIRN132 microRNA, humanMIRN132 microRNA, mouseMIRN134 microRNA, humanMirn134 microRNA, mouseReceptor, trkBRecombinant Proteinsactin cytoskeletonadriamycin nephropathybrain-derived neurotrophic factorpodocyte

Identifiers

PMID25408545
PMCPMC4356648
OpenAlexW1503091810

What OpenQuestion holds

Textmetadata
LicenceTDM
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.