Tier 3 — preclinical

Activation of tripartite motif-containing protein 16 improves cardiac function in aging mice by regulating Mfn2-dependent mitochondrial fusion through Sirt6

Yawu Chen, Hong Guo, Xiaochen Ding, Linhe Lu, Ping Jin
Cellular Signalling 2026 145:112573

Bibliography

PubMed
PMID 42086121
DOI
10.1016/j.cellsig.2026.112573

Study snapshot

DesignAged-mouse AAV intervention plus D-galactose cardiomyocyte mechanistic experiments.
ModelAged mice and D-galactose-treated H9c2 cardiomyocytes.
SampleMultiple animal and cellular experiments; exact group sizes not stated in indexed abstract.
InterventionIntracardiac AAV-TRIM16/Sirt6 manipulation.
DurationModel-specific.
EndpointsCardiac function; Myocardial fibrosis; Mitochondrial fusion; Mfn2; Mitochondrial respiratory capacity

What the study showed, in plain terms

In aged mice, activating the TRIM16-SIRT6 pathway improved heart function and mitochondrial fusion through Mfn2, supporting a role for SIRT6 in age-related cardiac mitochondrial maintenance.

Key findings

TRIM16 increased SIRT6 in the aging heart; TRIM16/SIRT6 promoted Mfn2-dependent mitochondrial fusion and respiratory capacity and improved cardiac function.

What this study can and cannot tell us

Mouse and cell evidence cannot establish that oral SIRT6 activators improve human heart failure or cardiac aging.

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Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability