Evidence map›Paper›PMID 42644150›Full record

ReviewLife metabolism2026

Stable clocks, rewired rhythms: circadian remodeling in skeletal muscle during aging, cachexia, and type 2 diabetes.

Francielly Morena, Mark R Viggars, Natalie Bohmke, Theodore E Ewachiw, Karyn A Esser

Abstract readReview
In one paragraph

Review in Life metabolism, 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

5 authors.

Francielly MorenaDepartment of Physiology and Aging, University of Florida, Gainesville, FL 32611, United States.ORCID https://orcid.org/0000-0001-5019-2125
Mark R ViggarsDepartment of Physiology and Aging, University of Florida, Gainesville, FL 32611, United States.ORCID https://orcid.org/0000-0002-0722-7051
Natalie BohmkeDepartment of Physiology and Aging, University of Florida, Gainesville, FL 32611, United States.ORCID https://orcid.org/0000-0002-6811-0615
Theodore E EwachiwDepartment of Physiology and Aging, University of Florida, Gainesville, FL 32611, United States.
Karyn A EsserDepartment of Physiology and Aging, University of Florida, Gainesville, FL 32611, United States.

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI Yenisel Cruz-Almeida · 2007 to 2026
$22.8M
Muscle clock and weakness: diversity supplementR01AR079220 · NIAMS · UNIVERSITY OF FLORIDA · PI ESSER, KARYN A · 2021 to 2025
$2.8M
Muscle Circadian Clock Disruption as a Cancer Cachexia ModifierF32AR085458 · NIAMS · UNIVERSITY OF FLORIDA · PI Francielly Morena Clark · 2025 to 2026
$150k
NIAMS NIH HHS F32 AR085458NIAMS NIH HHS R01 AR079220NIA NIH HHS P30 AG028740
6 · The paper itself

Abstract

In mammals, nearly every cell contains an intrinsic circadian clock that functions both as a timekeeping system and an environmental sensor, integrating external cues to maintain alignment between internal physiology and the external environment. While the core clock machinery is broadly conserved across tissues, its downstream rhythmic gene programs are highly tissue-specific and essential for maintaining cellular and physiological homeostasis. In the skeletal muscle, rhythmic program dysregulation has emerged as a common denominator in many unfavorable conditions. However, high-resolution circadian time-course studies in the muscle remain limited. In this review, we examine current evidence on the behavior of the skeletal muscle molecular clock and rhythmic transcriptional programs across aging, cancer-induced muscle atrophy (cachexia), and type 2 diabetes (T2D). Despite distinct pathological contexts, all three conditions undergo substantial condition-specific remodeling of the muscle rhythmic gene program, often converging on biological processes such as lipid metabolism and chromatin regulation. Collectively, available data suggest that circadian dysfunction in these conditions arises not from collapse of the core molecular oscillator but from progressive rewiring of rhythmic transcriptional programs despite relative preservation of core clock integrity. We discuss emerging mechanisms-including metabolic remodeling, glucocorticoid signaling, chromatin regulation, and noncanonical clock regulators-that may underlie this process. Moving forward, multi-omics studies integrating transcriptomic, proteomic, metabolomic, and epigenomic time-series analyses will be essential to distinguish mechanisms responsible for condition-specific rhythmic gene regulation. A clearer understanding of how rhythmic gene programs are rewired may reveal new opportunities to restore temporal coordination and improve skeletal muscle health across diverse pathological conditions.

Indexed as

atrophycircadianmusclerhythmic gene expressionsarcopenia

Identifiers

PMID42644150
PMCPMC13505632

What Socratic holds

Textmetadata
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.