Evidence map›Paper›PMID 39985671›Full record

ArticleCellular and molecular life sciences : CMLS2025

Class I PI3Ks activate stretch-induced autophagy in trabecular meshwork cells.

Myoung Sup Shim, Ethan J Sim, Kevin Betsch, Vaibhav Desikan, Chien-Chia Su, Diego Pastor-Valverde, Yang Sun, Paloma B Liton

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

8 authors.

Myoung Sup ShimDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA.
Ethan J SimDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA.
Kevin BetschDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA.
Vaibhav DesikanDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA.
Chien-Chia SuDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA.
Diego Pastor-ValverdeDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA.
Yang SunDepartment of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA, USA.
Paloma B LitonDepartment of Ophthalmology, Duke Eye Center, Duke University, AERI Bldg, Office 4004, Erwin, Rd. Box 3802, Durham, NC, 27713, USA. paloma.liton@dm.duke.edu.ORCID http://orcid.org/0000-0002-1440-3762

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Goldis Malek · 1985 to 2026
$19.3M
Autophagy and Mechanotransduction in the Trabecular MeshworkR01EY026885 · NEI · DUKE UNIVERSITY · PI Paloma Liton · 2016 to 2026
$4.7M
Autophagy and Retinal Ganglion Cell Death in GlaucomaR01EY033600 · NEI · DUKE UNIVERSITY · PI LITON, PALOMA · 2022 to 2025
$1.9M
BrightFocus Foundation G2022010SGlaucoma Research Foundation 2022NEI NIH HHS EY005722NEI NIH HHS EY026885NEI NIH HHS EY033600NEI NIH HHS P30 EY005722NEI NIH HHS R01 EY026885NEI NIH HHS R01 EY033600
6 · The paper itself

Abstract

Elevated intraocular pressure (IOP) is the primary risk factor for glaucoma, a leading cause of irreversible blindness worldwide. IOP homeostasis is maintained through a balance between aqueous humor production and its drainage through the trabecular meshwork (TM)/Schlemm's Canal (SC) outflow pathway. Prior studies by our laboratory reported a key role of mechanical forces and primary cilia (PC)-dependent stretch-induced autophagy in IOP homeostasis. However, the precise mechanism regulating this process remains elusive. In this study, we investigated the upstream signaling pathway orchestrating autophagy activation during cyclic mechanical stretch (CMS) in primary cultured human TM cells, using biochemical and cell biological analyses. Our results indicate that TM cells express catalytic subunits of class IA PI3Ks (PIK3CA, B, and D), and that inhibition of class IA isoforms, but not class II and III, significantly prevent CMS-induced autophagy. Importantly, PIK3CA was found to localize in the PC. Furthermore, we identified a coordinated action of Class IA PI3Ks along INPP4A/B, a 4' inositol phosphatase, responsible for the formation of PI(3,4)P

Indexed as

AutophagyClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesTrabecular MeshworkCells, CulturedCiliaHumansIntraocular PressurePhosphoric Monoester HydrolasesSignal TransductionStress, MechanicalClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesPIK3CA protein, humanAutophagyGlaucomaMechanical stressPI3KPrimary ciliaTrabecular meshwork

Identifiers

PMID39985671
PMCPMC11846827

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.