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Hallmarks of aging
Research brief

Calcium overload and NFAT signaling in impaired skeletal muscle regeneration

In this abstract, calcium overload kept myoblasts proliferating and suppressed myogenic markers via NFAT signaling; an NFAT inhibitor restored myotube formation in vitro. [1]

Automatic summary · not editorially reviewed

The key findings

  1. Transcriptomic analysis of aged human muscle showed coordinated activation of calcium signaling and proliferation pathways. [1]

  2. In vitro, calcium exposure increased myoblast proliferation under differentiation conditions while suppressing myogenic markers. [1]

  3. The NFAT inhibitor VIVIT prevented calcium-induced NFATc1 nuclear accumulation and restored myotube formation in vitro. [1]

The source at a glance

Study type / format
Abstract of a laboratory and tissue study
Population / context
Aged human muscle tissue, cultured myoblasts, ovariectomized mice and human calcific tendinitis tissue.
Summary based on
Study abstract
Original publication
October 2, 2026

Aged human muscle and calcium–proliferation pathways

The study asked how calcium dysregulation affects muscle regeneration. Transcriptomic analysis of aged human muscle showed coordinated activation of calcium signaling and proliferation pathways. The abstract does not report sample size, participant details or how aged was defined.

Supporting source [1]

Myoblasts in vitro and mouse and tendon tissue findings

In vitro, calcium exposure increased myoblast proliferation under differentiation conditions while suppressing myogenic markers. RNA sequencing showed upregulated proliferative programs, suppressed myogenic genes and enriched calcium-NFAT signaling. Calcium promoted NFATc1 nuclear translocation and raised Ccnd1 expression. Ovariectomized mice, described as having systemic calcium dysregulation, and human calcific tendinitis tissue, described as localized calcium overload, showed NFAT-associated proliferative signatures with suppressed myogenic markers.

Supporting source [1]

NFAT inhibitor VIVIT and study limits

The selective NFAT inhibitor VIVIT prevented calcium-induced NFATc1 nuclear accumulation and restored myotube formation in vitro; in an in vivo injury model it promoted myofiber maturation. The authors conclude that chronic calcium-NFAT signaling may link calcium dysregulation to impaired muscle regeneration. These are abstract-level findings; the full text was not reviewed, and the abstract does not report sample sizes, follow-up or effect sizes.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. The abstract does not report sample sizes, participant details, follow-up or effect sizes. Findings are associations and preclinical results, not proven human benefits.

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

Source & supporting passages

[1]
Pathological calcium overload impairs skeletal muscle regeneration through sustained NFAT-dependent proliferative signaling.

Lee S, Cho N, Jo S, Ji JH, Kim JO, Park C, Choi S, Kim EM, Kim KK. · europepmc.org · October 2, 2026

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

    Transcriptomic analysis of aged human muscle revealed
  2. Finding 2 ↑

    increased myoblast proliferation under differentiation conditions
  3. Finding 3 ↑

    VIVIT prevented calcium-induced NFATc1 nuclear accumulation

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

Our editorial method

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