Aging-related myocardial susceptibility and chronic intermittent hypoxia in mice and senescence-like cardiomyocytes
In mice and senescence-like cardiomyocytes, pre-existing aging-related myocardial susceptibility amplified chronic intermittent hypoxia-induced cardiac injury; Drp1 knockdown only partly restored mitochondrial measures. [1]
Automatic summary · not editorially reviewed
The key findings
The study used G3 Tert-deficient mice and D-galactose-induced senescence-like primary cardiomyocytes to test aging-related myocardial susceptibility to chronic intermittent hypoxia. [1]
Compared with CIH alone, ejection fraction and fractional shortening were reduced by an additional 24.6% and 15.8%, respectively. [1]
Drp1 knockdown restored 55.1% of the CIH plus D-galactose-induced ATP decline and reversed 47.4% of the mitochondrial reactive oxygen species excess. [1]
The source at a glance
- Study type / format
- Preclinical animal and cell study (abstract).
- Population / context
- G3 Tert-deficient mice, young wild-type mice and D-galactose-induced senescence-like primary cardiomyocytes.
- Summary based on
- Study abstract
- Original publication
- September 1, 2026
Aging-related susceptibility in mice and cells under hypoxia
The abstract asks whether a pre-existing aging-related myocardial susceptibility lowers the tolerance threshold for chronic intermittent hypoxia (CIH), a feature of obstructive sleep apnea, and whether Dynamin-related protein 1 (Drp1) contributes to greater vulnerability of senescence-like cardiomyocytes. The work used G3 Tert-deficient mice and D-galactose-induced senescence-like primary cardiomyocytes. In young wild-type mice, 8 weeks of CIH caused early cardiac remodeling and senescence-associated myocardial stress without overt systolic decompensation. In Tert mice, the same CIH exposure shifted the response further toward maladaptive remodeling.
Supporting source [1]
Ejection fraction and mitochondrial findings with Drp1 knockdown
Compared with CIH alone, ejection fraction (EF) and fractional shortening (FS) were reduced by an additional 24.6% and 15.8%, respectively. In senescence-like cardiomyocytes, CIH amplified mitochondrial vulnerability, with impaired energy production, elevated mitochondrial oxidative stress and a fission-biased mitochondrial dynamics marker profile. Drp1 knockdown did not fully reverse this mitochondrial state: it restored 55.1% of the CIH plus D-galactose-induced ATP decline and reversed 47.4% of the mitochondrial reactive oxygen species excess, while attenuating DNA damage response activation and senescence-associated signaling.
Supporting source [1]
Interpretation of Drp1-linked mitochondrial dynamics in this abstract
The authors conclude that aging-related myocardial susceptibility is not a passive contextual factor in CIH-induced injury but a biological state that actively shapes the cardiac response to repeated hypoxia-reoxygenation stress. They suggest that Drp1-associated mitochondrial dynamics imbalance may represent a functional link between diminished mitochondrial stress tolerance and amplified cardiomyocyte vulnerability. These are interpretations of mouse and cell experiments; the abstract reports no human outcomes, and the partial restoration after Drp1 knockdown indicates that other factors also contribute.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from mice and senescence-like primary cardiomyocytes, not human outcomes. The abstract reports no sample sizes, no follow-up beyond the stated 8 weeks of CIH, and no details on blinding or randomization. Drp1 knockdown did not fully reverse the mitochondrial state, so the reported links are partial and associative rather than established causal mechanisms in humans.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Su Y, Miao Y, Tan J, Wang F, Zhang Q. · europepmc.org · September 1, 2026