Review: age-related loss of calcium signaling fidelity and mitochondrial dysfunction
This review abstract describes how aging destabilizes intracellular calcium signaling in neurons and skeletal muscle, converging on mitochondrial dysfunction, senescence and cognitive-motor decline; it proposes therapeutic strategies but reports no tested outcomes. [1]
Automatic summary · not editorially reviewed
The key findings
The abstract states that calcium signaling versatility depends on coordinated channels, pumps, exchangers, buffering proteins and organelle contact sites forming microdomains. [1]
According to the abstract, these calcium alterations converge on mitochondrial dysfunction, a central hallmark of aging, leading to senescence and impaired tissue adaptation. [1]
The review examines therapeutic strategies aimed at restoring calcium signaling fidelity as potential interventions to preserve tissue function and extend healthspan. [1]
The source at a glance
- Study type / format
- Review abstract
- Population / context
- Neuronal and skeletal muscle systems discussed in an aging review
- Summary based on
- Study abstract
- Original publication
- September 14, 2026
Calcium signaling toolkit across tissues
The abstract states that calcium controls essential functions in virtually every tissue. Its versatility depends on precise spatial and temporal coordination of channels, pumps, exchangers, buffering proteins and organelle contact sites that form organized intracellular calcium microdomains. During aging, the abstract says this signaling quality progressively deteriorates.
Supporting source [1]
Mitochondria, senescence and nervous system
According to the abstract, altered plasma membrane channel activity, defective endoplasmic reticulum calcium handling, impaired mitochondrial buffering, oxidative stress and chronic inflammation destabilize calcium homeostasis. These changes converge on mitochondrial dysfunction, described as a central hallmark of aging, leading to bioenergetic decline, excessive reactive oxygen species, cellular senescence and impaired tissue adaptation. In the nervous system, disrupted calcium signaling is said to contribute to synaptic dysfunction, neuroinflammation and neuronal vulnerability linked to cognitive decline and neurodegenerative disease.
Supporting source [1]
Skeletal muscle and proposed strategies
In skeletal muscle, the abstract says defective calcium handling impairs excitation-contraction coupling, mitochondrial metabolism and regenerative capacity, thereby promoting sarcopenia and motor decline. The review examines therapeutic strategies aimed at restoring calcium signaling fidelity as potential interventions to preserve tissue function and extend healthspan. These are proposed approaches; the abstract reports no tested interventions or outcomes.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. It describes proposed mechanisms and therapeutic strategies without reporting study design, sample, follow-up or tested outcomes. Associations described are not established causes, and proposed interventions are not validated treatments.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Linsambarth S, Lopez-Moroni A, Casanova C, Alarcon S, Araos L, Puebla-Huerta A, Jaña F, Lovy A, Villalobos C, Cárdenas JC. · europepmc.org · September 14, 2026