ArticleJournal of neuroinflammation2026
CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain.
Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
High-fat diets represent a primary factor driving the global obesity epidemic, thereby constituting a substantial public health challenge. Previous research has demonstrated that obese individuals exhibiting a higher prevalence of pain-related disorders. However, the underlying neural mechanisms involved remain largely unknown. Here, we identified that glutamatergic neurons in the paraventricular thalamus (PVTGlu) nucleus are involved in obesity-related pain. Inhibition of PVTGlu neurons reversed the pain hypersensitivity in obese mice. Proteomic analysis of plasma samples from obese patients revealed a marked increase in the level of the chemokine (C-X-C motif) ligand 7 (CXCL7). Infusion of CXCL7 into the PVT increased the excitability of PVTGlu neurons and induced pain hypersensitivity in control mice. In addition, increased expression of the CXC chemokine receptor 2 (CXCR2) receptor was observed in PVTGlu neurons of obese mice. Knockdown of CXCR2 receptors in the PVTGlu neurons attenuated PVTGlu neuronal excitability and relieved pain hypersensitivity in obese mice. Furthermore, PVTGlu neurons send excitatory inputs to glutamatergic neurons in the basolateral amygdala (BLAGlu) that are required for obesity-related pain. Our study demonstrates that downregulation of CXCR2 receptors in the PVTGlu neurons abrogated the rise in BLAGlu neuronal activity while alleviating pain hypersensitivity in obese mice. Collectively, these findings emphasize the critical involvement of the CXCL7-CXCR2 axis enhances PVTGlu → BLAGlu pathway in obesity-related pain hypersensitivity, providing novel insights for the development of therapeutic strategies targeting obesity-related pain.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.