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Hallmarks of aging
Research brief

Human and mouse muscle studies link fibre atrophy to fewer myofibrils

In young and older humans and in mice, radial atrophy of muscle fibres during ageing and disuse was mainly associated with a lower number of myofibrils rather than smaller myofibrils. [1]

Automatic summary · not editorially reviewed

The key findings

  1. Skeletal muscle structure was assessed at macroscopic, microscopic and ultrastructural levels in young and older humans and mice, including a mouse unilateral immobilization model of disuse. [1]

  2. Human ageing was associated with radial atrophy of SERCA1-positive fibres, largely explained by fewer myofibrils rather than smaller myofibrils, while SERCA2-positive fibre cross-sectional area was preserved. [1]

  3. In mice, disuse caused radial fibre atrophy almost exclusively associated with a lower number of myofibrils. [1]

The source at a glance

Study type / format
Abstract of a study combining human and mouse muscle analyses
Population / context
Young and older humans and young and old mice, as described in the abstract.
Summary based on
Study abstract
Original publication
September 25, 2026

Muscle structure in young and older humans and mice

The abstract describes a study of skeletal muscle structure at macroscopic, microscopic and ultrastructural levels in young and older humans and mice. In humans, magnetic resonance imaging measured quadriceps muscle volume and cross-sectional area, while vastus lateralis biopsies were examined with standard immunohistochemistry and a fluorescence imaging pipeline for ultrastructural analysis. Parallel mouse experiments included a unilateral immobilization model of disuse-induced atrophy. The authors state that whether radial fibre atrophy is driven mainly by smaller myofibrils or by loss of myofibrils had remained unanswered.

Supporting source [1]

Fewer myofibrils in aged human and mouse fibres

Ageing in humans was associated with lower muscle volume and cross-sectional area and with radial atrophy of SERCA1-positive fibres, whereas the cross-sectional area of SERCA2-positive fibres was preserved. The radial atrophy of SERCA1 fibres was largely explained by a lower number of myofibrils rather than a smaller size of the myofibrils. Aged mice showed similar alterations, although SERCA1 fibres there also had slightly smaller myofibrils. These are associations in the described samples, not proof that myofibril loss causes atrophy.

Supporting source [1]

Disuse atrophy in mice and the abstract's limits

In mice, disuse likewise caused radial muscle fibre atrophy that was again almost exclusively associated with a lower number of myofibrils. The authors conclude that loss of myofibrils is a central and conserved mechanism mediating radial fibre atrophy during ageing and disuse and call it a potential therapeutic target for preserving skeletal muscle mass. This is an abstract only; the full text was not reviewed. Sample sizes, follow-up periods and detailed statistics are not reported here, and the therapeutic-target statement is a proposal, not a demonstrated treatment.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. Sample sizes, follow-up and detailed statistics are not reported, and the findings are associations, not proven causes or treatments.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

[1]
Macroscopic to ultrastructural analyses identify the loss of myofibrils as the primary mediator of ageing- and disuse-induced muscle fibre atrophy.

Sayed RKA, Lange AN, Paez HG, Hibbert JE, Meinhold M, Flynn CGK, Hartung J, Santibanez MBZ, Dobrzycki I, Wrucke DJ, Zepeda CS, James JJ, Sundberg CW, Hornberger TA. · europepmc.org · September 25, 2026

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    young and older humans and mice
  2. Finding 2 ↑

    lower number of myofibrils, rather than a
  3. Finding 3 ↑

    almost exclusively associated with a lower number

AI-assisted summary with linked source passages. No independent editorial or clinical review.

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