Evidence map›Paper›PMID 41937554›Full record

ArticleEndocrinology and metabolism (Seoul, Korea)2026

Muscle Loss Driven by Extracellular Signal-Regulated Kinase Suppression via β-Adrenergic Activation in High-Normal Catecholamine Status.

Jieun Lee, Ju Yeon Kwak, Ho Yeop Lee, Ji Sun Moon, Hyo Ju Jang, Ha Thi Nga, Thi Linh Nguyen, Alfin Mohammad Abdillah, Junglyun Kim, Sihwan Kim and 3 more

Abstract read
In one paragraph

Article in Endocrinology and metabolism (Seoul, Korea), 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

13 authors.

Jieun Lee *Laboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Ju Yeon Kwak *Laboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Ho Yeop LeeLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Ji Sun MoonLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Hyo Ju JangLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Ha Thi NgaLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Thi Linh NguyenLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Alfin Mohammad AbdillahLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea.
Junglyun KimChungnam National University College of Nursing, Daejeon, Korea.
Sihwan KimDepartment of Applied Bioengineering, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, Korea.
Yong Ryoul YangAging Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Jeong Eun LeeDepartment of Radiology, Chungnam National University Hospital, Daejeon, Korea. nasa80@cnuh.co.kr.
Hyon-Seung YiLaboratory of Endocrinology and Immune System, Chungnam National University College of Medicine, Daejeon, Korea. jmpbooks@cnu.ac.kr.

Funding

Korea Health Industry Development InstituteMinistry of Health and Welfare RS-2022-KH130308Ministry of Health and Welfare RS-2024-00507183Ministry of Science and ICTMinistry of Science, ICT and Future PlanningNational Research Council of Science and Technology CRC22011-200National Research Foundation of Korea 2021R1A5A8029876National Research Foundation of Korea 2023R1A2C3006220
6 · The paper itself

Abstract

backgruoundCatecholamines play a crucial role in muscle biogenesis, but their persistent elevation is linked to muscle wasting, which is poorly understood. This study aimed to investigate the association between catecholamine levels and age-related muscle loss.

methodsThis retrospective study evaluated the plasma levels of two catecholamines, metanephrine and normetanephrine, and the clinical characteristics of 830 patients with adrenal incidentaloma on computed tomography (CT). Cross-sectional CT data at the L3 lumbar vertebrae were used to measure muscle areas. In vitro studies on C2C12 myotubes were conducted to examine β-adrenergic receptor signaling pathways and their role in myogenesis.

resultsMen had significantly higher mean metanephrine levels of 0.17 nmol/L and normetanephrine levels of 0.63 nmol/L than women (P<0.05). Total abdominal muscle area was negatively correlated with catecholamine levels in both men and women, with the strongest negative correlation between normetanephrine levels and total abdominal muscle area in men (r=-0.31, P<0.001). Similarly, the strongest negative correlation between visceral fat area and metanephrine was observed in men (r=-0.25, P=0.004). Clenbuterol, a β-adrenergic receptor agonist, inhibited myogenesis, including myotube formation by extracellular signal-regulated kinase (ERK) suppression in C2C12 myoblasts. Conversely, β-blockers increased myogenesis via increasing ERK phosphorylation in C2C12 cells. These findings suggest that β-adrenergic modulation influences skeletal muscle differentiation, with ERK phosphorylation.

conclusionCatecholamine levels are associated with age, sex, muscle mass, and fat mass. Monitoring catecholamine levels, particularly in older men and in individuals with reduced muscle mass, may help manage age-related muscle loss and lead to individualized treatment strategies.

Indexed as

CatecholaminesExtracellular Signal-Regulated MAP KinasesMetanephrineMuscle, SkeletalMuscular AtrophyNormetanephrineReceptors, Adrenergic, betaAdrenal Gland NeoplasmsAgedAnimalsCross-Sectional StudiesFemaleHumansMaleMiceMiddle AgedCatecholaminesExtracellular Signal-Regulated MAP KinasesMetanephrineNormetanephrineReceptors, Adrenergic, betaCatecholaminesMuscle developmentMusclesβ-Adrenergic signaling

Identifiers

PMID41937554
PMCPMC13172642

What Socratic holds

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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 Socratic graph.