TheriogenologyOct 6, 2026

SIRT2 helps fix damaged mitochondria in older cow egg cells by changing SQSTM1 at a specific site

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 7, 2026

Abstract

SIRT2 protein levels were significantly down-regulated in aged bovine oocytes.

Aging in female breeding cows is associated with defects in oocyte maturation and mitochondrial function.
Microinjection of SIRT2 mRNA improved maturation outcomes in aged bovine oocytes.
Restoration of mitochondrial function and mitophagy was observed following SIRT2 mRNA treatment.
SIRT2 is involved in modifying a protein called SQSTM1, which affects the degradation of damaged mitochondria.
The decrotonylation of SQSTM1 enhances its interaction with another protein, LC3B, promoting the removal of aged mitochondria.

Simplified

Aging-associated defects in oocyte in vitro maturation limit the applications of assisted reproductive technologies in aged females breeding cows. In this study, SIRT2 protein levels were significantly down-regulated in aged bovine oocytes, accompanied by impaired mitochondrial function. Microinjection of SIRT2 mRNA ameliorated maturation failure in aged bovine oocytes, while restoring mitochondrial function and mitophagy. Mechanistically, we demonstrated that SIRT2 mediated the decrotonylation of SQSTM1 at lysine 100. Decrotonylation of SQSTM1 at K100 facilitated its interaction with LC3B, thereby accelerating lysosomal degradation of age-associated damaged mitochondria. Consistently, SQSTM1 decrotonylation at lysine 100 enhanced mitophagy and rescued maturation defects in maternally aged oocytes, and this protective effect was independent of SQSTM1 hypercrotonylation. Our findings reveal a novel mechanism underlying oocyte aging and identify a promising molecular target for improving oocyte maturation in aged elite cattle.

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SIRT2 helps fix damaged mitochondria in older cow egg cells by changing SQSTM1 at a specific site

Abstract

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