Evidence map›Paper›PMID 41781352›Full record

ArticleBritish journal of pharmacology2026

The β

Kristan H Cleveland, Kyung-Soon Lee, Devasena Ponnalagu, Juan Jesus Vicente, Edward D Parker, Ji Yae Eunice Lee, Linda Wordeman, John D Scott

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of pharmacology, 2026. 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

8 authors.

Kristan H ClevelandDepartment of Pharmacology, University of Washington, Seattle, Washington, USA.
Kyung-Soon LeeDepartment of Pharmacology, University of Washington, Seattle, Washington, USA.
Devasena PonnalaguDepartment of Pharmacology, University of Washington, Seattle, Washington, USA.
Juan Jesus VicenteDepartment of Neurobiology and Biophysics, University of Washington, Seattle, Washington, USA.
Edward D ParkerDepartment of Opthamology, University of Washington, Seattle, Washington, USA.
Ji Yae Eunice LeeDepartment of Pharmacology, University of Washington, Seattle, Washington, USA.
Linda WordemanDepartment of Neurobiology and Biophysics, University of Washington, Seattle, Washington, USA.
John D ScottDepartment of Pharmacology, University of Washington, Seattle, Washington, USA.

Funding

Vision Research CoreP30EY001730 · NEI · UNIVERSITY OF WASHINGTON · PI Jay Neitz · 1985 to 2026
$23.5M
Diabetes, Obesity and Metabolism Training ProgramT32DK007247 · NIDDK · UNIVERSITY OF WASHINGTON · PI GREGORY J MORTON, KRISTINA Marie UTZSCHNEIDER · 1986 to 2026
$10.0M
Defective PKA Signaling in Cushing's SyndromeR01DK119192 · NIDDK · UNIVERSITY OF WASHINGTON · PI John D Scott · 2018 to 2026
$4.4M
Microtubule dynamics and error correctionR01GM145567 · NIGMS · UNIVERSITY OF WASHINGTON · PI WORDEMAN, LINDA · 2022 to 2025
$1.8M
Biased AKAP signaling mechanismsR01DK141129 · NIDDK · UNIVERSITY OF WASHINGTON · PI John D Scott · 2024 to 2026
$1.7M
NEI NIH HHS P30 EY001730NEI NIH HHS P30-EY001730NIDDK NIH HHS R01 DK119192NIDDK NIH HHS R01DK119192-07NIDDK NIH HHS R01 DK141129NIDDK NIH HHS R01DK141129-01NIDDK NIH HHS T32 DK007247NIGMS NIH HHS R01 GM145567NIGMS NIH HHS R01GM145567NIH Diabetes, Obesity, and Metabolism program of the National Institutes of Health T32DK007247-46
6 · The paper itself

Abstract

background and purposeSignal transduction therapies aim to correct dysregulated cellular signalling pathways implicated in disease. Adrenal Cushing's syndrome, a disorder of excess cortisol production, is frequently driven by somatic mutations in protein kinase A catalytic subunits (PKAc), including PKAc EXPERIMENTAL APPROACH: This study used a combination of in vitro adrenal cell models and an in vivo mouse model harbouring the PKAc W196R mutation to assess the effects of formoterol treatment on mitochondrial function, steroidogenic gene expression and cortisol production. Mitochondrial respiration was evaluated by Seahorse XF analysis and serial block face scanning electron microscopy, and protein expression was measured by western blot and immunohistochemistry. KEY

resultsIn this study, we demonstrate that the long-acting β CONCLUSION AND IMPLICATIONS: These findings support the therapeutic potential of formoterol as a new pharmacological strategy for treating Cushing's syndrome and its associated metabolic comorbidities.

Indexed as

Adrenergic beta-2 Receptor AgonistsCushing SyndromeFormoterol FumarateAnimalsCell LineCorticosteroneCyclic AMP-Dependent Protein KinasesHumansMaleMiceMitochondriaAdrenergic beta-2 Receptor AgonistsCorticosteroneCyclic AMP-Dependent Protein KinasesFormoterol Fumarateadrenal glandCushing's syndromemitochondriaprotein kinase Aβ2‐adrenoceptor

Identifiers

PMID41781352
PMCPMC13138844

What Socratic 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 Socratic graph.