Activating the PGC-1 α /TERT Pathway by Catalpol Ameliorates Atherosclerosis via Modulating ROS Production, DNA Damage, and Telomere Function: Implications on Mitochondria and Telomere Link.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and in vitro study without human data.
PubMed 30046372 · doi:10.1155/2018/2876350
What was done
Researchers investigated the effects of catalpol (an iridoid glucoside from Rehmannia glutinosa L.) on atherosclerosis, oxidative stress, DNA damage, and telomere shortening in LDLr -/- mice. They also evaluated oxidized LDL-treated macrophages transfected with PGC-1α or TERT siRNA to assess pathway involvement, and measured PGC-1α promoter activity using a dual-luciferase reporter assay.
What was found
The abstract reports no numerical values, sample sizes, or effect estimates. The authors reported that catalpol reduced atherosclerosis, oxidative stress, DNA damage, and telomere shortening in LDLr -/- mice. In oxLDL-treated macrophages, catalpol lowered oxidative stress and DNA damage while preserving telomere function via the PGC-1α/TERT pathway, and directly enhanced PGC-1α promoter activity.
Why it matters
This work identifies the PGC-1α/TERT pathway connecting mitochondrial function and telomere maintenance as a potential target in atherosclerosis and provides a mechanistic basis for catalpol in preclinical models.
Limits
The study is entirely preclinical, relying on a mouse knockout model and cell cultures that may not reflect human disease. The abstract provides no sample sizes, dosages, treatment durations, or quantitative outcome measures.
Cited by
- supports Research demonstrates a feedback loop between mitochondria and telomere length, with telomerase reverse transcriptase repairing mitochondria by reducing oxidative stress.