Evidence map›Paper›PMID 41460555›Full record

ArticleMolecular neurobiology2025

Selective Receptor Modulation by Truncated Neuropeptide Y (3-36) Dissociates Vasoconstriction from Neuroprotection in Experimental Glaucoma.

Viswanthram Palanivel, Devaraj Basavarajappa, Akanksha Salkar, András M Komáromy, Ole Tietz, Taslima Akter Eva, Nitin Chitranshi, Mehdi Mirzaei, Veer Gupta, Yuyi You and 2 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

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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

12 authors.

Viswanthram Palanivel *Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. viswa.palanivel@mq.edu.au.
Devaraj BasavarajappaMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Akanksha SalkarMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
András M KomáromyDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, MI, USA.
Ole TietzDementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Taslima Akter EvaMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Nitin ChitranshiMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Mehdi MirzaeiMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Veer GuptaSchool of Medicine, Deakin University, Geelong, VIC, 3216, Australia.
Yuyi YouMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Stuart L GrahamMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia.
Vivek Gupta *Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. vivek.gupta@mq.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropeptide Y (NPY) is a multifunctional peptide with neuroprotective properties, but its therapeutic use in the retina and optic nerve may be limited by vasoconstrictive effects mediated through Y1 receptor activation. This study evaluated the vascular effects of full-length NPY (1-36) and its N-terminally truncated analog, NPY (3-36), in the mouse retina. Retinal vascular responses were assessed using fluorescein angiography (FFA) after intravitreal administration of different NPY analogs. NPY (1-36) caused transient vasoconstriction via Y1 receptor-mediated calmodulin and pMLC activation. In contrast, NPY (3-36) selectively activates Y2 and Y5 receptors without inducing vasoconstrictive effects. Furthermore, NPY (3-36) through receptor activation preserved retinal ganglion cell density, axonal integrity, and inner retinal function while reducing astrocytic and microglial activation under elevated intraocular pressure. These findings suggest that NPY (3-36) could be a safer therapeutic candidate for glaucoma, highlighting the critical role of receptor-specific modulation to enhance neuroprotection without causing adverse vascular complications.

Indexed as

GlaucomaNeuropeptide YNeuroprotectionNeuroprotective AgentsReceptors, Neuropeptide YVasoconstrictionAnimalsDisease Models, AnimalIntraocular PressureMaleMiceMice, Inbred C57BLMicrogliaRetinal Ganglion CellsNeuropeptide YNeuroprotective AgentsReceptors, Neuropeptide YGlaucomaNeuropeptide YNeuroprotectionNPY (3–36)Vasoconstriction

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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.