Key result
PPARγ agonists alleviate periostin-induced arterial calcification by reversing abnormal glycolysis and mitochondrial damage.
Why the study?
The mechanisms by which periostin promotes arterial calcification and its relationship with glucose metabolism and mitochondrial function were unclear.
Periostin promotes arterial calcification through metabolic reprogramming, and PPARγ agonists may offer a therapeutic strategy to alleviate this process.
Periostin may promote arterial calcification via metabolic stress; animal data leave open whether PPARγ agonists offer a viable human therapy.
Periostin caused arterial calcification, overactivated glycolysis, and damaged OXPHOS. PPARγ agonists alleviated periostin-promoted arterial calcification and corrected abnormal glycolysis and unbalanced mitochondrial homeostasis. There exists a relationship between periostin and lactate in patients with CAC.
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Zhu et al. (2021) studied this question. Periostin promotes arterial calcification through abnormal glycolysis and mitochondrial damage, effects alleviated by PPARγ agonists and correlated with lactate in patients.
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