Evidence map›Paper›PMID 40758097›Full record

ReviewBiomolecules & biomedicine2025

Neuropeptide S pathway in PTSD and neuropsychiatric disorders: A review.

Zhi-Cheng Zhu, Xue-Jing Han, Zhen He, Meng-Yang Liu, Ning Wu, Xiang-Min Tong, Fei Li

Abstract readReview
In one paragraph

Review in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Zhi-Cheng ZhuBeijing Institute of Pharmacology and Toxicology, Beijing, China; Department of Pharmacology, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Xue-Jing HanBeijing Institute of Pharmacology and Toxicology, Beijing, China; Department of Pharmacy, Shenyang Pharmaceutical University, Shenyang, Liaoning, China.
Zhen HeBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Meng-Yang LiuBeijing Institute of Pharmacology and Toxicology, Beijing, China; Department of Pharmacy, Shenyang Pharmaceutical University, Shenyang, Liaoning, China.
Ning WuBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Xiang-Min TongDepartment of Hematology, Zhejiang Provincial People's Hospital and People's Hospital of Hangzhou Medical College, Hangzhou, China.
Fei LiBeijing Institute of Pharmacology and Toxicology, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-traumatic stress disorder (PTSD) is a multidimensional illness that seldom occurs alone: roughly 80 % of patients also meet criteria for anxiety, depression, chronic pain, substance-use, eating or cognitive disorders. Converging genetic, neurochemical and behavioural findings implicate the neuropeptide S (NPS) system-acting through its G-protein-coupled NPS receptor (NPSR)-as a common regulator of these diverse phenotypes. This narrative review surveys studies published 2000-2024 in PubMed, Embase and Web of Science that examine NPS/NPSR involvement in core PTSD features and typical comorbidities. The functional rs324981 A/T polymorphism, which boosts NPSR surface expression and signalling, consistently associates with greater PTSD risk and symptom severity. In rodent models, exogenous NPS reduces anxiety- and fear-like behaviours, speeds fear-memory extinction, stabilises the hypothalamic-pituitary-adrenal axis, enhances dopaminergic tone and elevates hippocampal brain-derived neurotrophic factor (BDNF)-changes concordant with symptom relief. Additional work shows that NPS lessens pain affect, dampens alcohol and opioid intake, eases withdrawal-induced anxiety and lowers food consumption, hinting at a multimodal therapeutic profile. These effects converge on limbic and mid-brain circuits (amygdala, ventral tegmental area, locus coeruleus, paraventricular nucleus) and engage oxytocinergic, adenosinergic and endocannabinoid pathways. Translation remains limited by NPS's rapid degradation, poor blood-brain-barrier penetration and scarcity of brain-penetrant NPSR ligands, but advances in intranasal delivery, lipid-acylated analogues, biased NPSR agonists and "humanised" NPSR-variant models offer promising solutions. Collectively, current pre-clinical and genetic evidence positions the NPS-NPSR axis as a versatile therapeutic target for both core PTSD symptoms and their disabling comorbidities, warranting rigorous translational studies to refine mechanism, optimise drug-like properties and test clinical efficacy.

Indexed as

Mental DisordersNeuropeptidesStress Disorders, Post-TraumaticAnimalsHumansReceptors, G-Protein-CoupledSignal TransductionNeuropeptidesneuropeptide S, humanReceptors, G-Protein-Coupled

Identifiers

PMID40758097
PMCPMC12505535

What Socratic holds

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LicenceCC BY
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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.