From: Sirtuins in intervertebral disc degeneration: current understanding
Authors (reference) | Type of study | Study design | Aim | Results | Conclusion |
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Kanwal et al. (2019) | An experimental study | Experimental in vivo study | To determine the role of Sirt6 and mitochondrial Sirt (Sirt3)in protecting a diabetic heart from developing cardiomyopathy | In cardiomyocytes, Sirt6 downregulates Keap1 expression and inhibits the binding of Kelch-like ECH-associated protein 1 (Keap1) to Nrf2, thereby stabilizing Nrf2 and activating the transcription of Nrf2-dependent genes, including Sirt3 | Sirt6 and Sirt3 regulate each other's activity, which may be critical for coordinating cellular metabolism and maintaining the health of an organism |
Kuno et al. (2023) | An experimental study | Experimental in vivo and in vitro study | To investigate whether SIRT1 counteracts doxorubicin-induced cardiotoxicity by mediating the phosphorylation of Ser139 of histone H2AX, a key signal in the DNA damage response | 1) endogenous SIRT1 protein in cardiomyocytes counteracts doxorubicin-induced cardiotoxicity.2) SIRT1 mediates the DDR and protects cells from apoptosis by regulating histone H2AX phosphorylation via its deacetylation | SIRT1 counteracts doxorubicin-induced cardiotoxicity by mediating H2AX phosphorylation through its deacetylation in cardiomyocytes |
Lin et al. (2023) | An experimental study | Experimental in vivo and in vitro study | Discovery of a mechanism by which hepatocyte SIRT2 regulates hepatic bone crosstalk | In SIRT2-deficient hepatocytes, LRG1 levels in sEVs are upregulated, leading to increased transfer of LRG1 to bone-marrow-derived monocytes (BMDMs), and in turn, to inhibition of osteoclast differentiation via reduced nuclear translocation of NF-κB p65 | Hepatocyte SIRT2 regulates pro-osteoclast signaling of NF-κB p65 in osteoblasts via the sEV-LRG1 pathway |