SIRT5 (Sirtuin 5)

Finally, we also documented an increase in mitochondria reactive oxygen species (mtROS). The combined inhibition of SIRT3 and activation of SIRT5 greatly reduces the size of spheroids through the inhibition of hypoxic response, which is then followed by the alteration of the autophagic and mitophagic process and the toxic accumulation of mitochondrial ROS, representing a new anti-tumoral strategy.

Our study provides a high-resolution molecular map of human skin aging, demonstrating that UV radiation does not merely accelerate but fundamentally rewires the aging network, driving pathways distinct from intrinsic aging. Key identified drivers include sirtuin depletion, aberrant stress signaling, and a chronic pseudo-inflammatory response, offering novel targets for anti-photoaging interventions.

SIRT6 overexpression was linked to favorable prognosis in esophageal carcinoma and sarcoma, while unfavorable outcomes were observed in hepatocellular carcinoma and cholangiocarcinoma. SIRT7 upregulation was significantly associated with reduced survival in esophageal, liver, and uterine cancers, but surprisingly correlated with improved outcomes in urothelial carcinoma and cervical squamous cell carcinoma.ConclusionsTogether, this multi-omics analysis reveals the correlation and prognostic values of sirtuins across multiple types of human cancers and suggests that sirtuins may serve as promising biomarkers for different cancers.

Given its unique post-translational modification activity and biological and physiological functions, SIRT5 has recently emerged as a promising therapeutic target against liver diseases. In this review, we summarize the current knowledge regarding SIRT5 in liver diseases to provide a comprehensive understanding of the research progress of SIRT5 in liver diseases.

The potential NARH binding site is further investigated using a suite of biochemical and computational approaches. The current study provides greatly needed mechanistic understanding of SIRT5 regulation, as well as a novel chemical scaffold for further activator development.

Our study reveals that SIRT5-mediated CTBP1 succinylation drives HCC progression through MAT1A suppression, establishing a novel regulatory axis with therapeutic potential for HCC treatment.

METTL14 stabilizes SIRT5 mRNA via m6A modification, upregulating SIRT5 expression and inducing ferroptosis, thereby inhibiting GC progression.

AA induces ferroptosis in HCC through the SIRT5-ACSL4/LPCAT3/ALOX15 pathway, offering mechanistic insight into lipid metabolism-related ferroptotic regulation.

The data from the CTRP database and the Cell Counting Kit-8 (CCK-8) experiment suggested that SIRT1 increased the sensitivity of B-ALL cell lines to vincristine. In vitro experiments demonstrated that SIRT1 inhibits invasion activity in B-ALL cell lines (NALM6 and REH). SIRT1 represents a potential prognostic biomarker and therapeutic target in childhood B-ALL.

This study presents the first comprehensive Kla landscape in PCa, suggesting its potential regulatory role in tumor progression. These findings provide a valuable resource for future studies and support Kla as a possible target for therapeutic intervention in prostate cancer.

This study quantified the dynamic changes in protein succinylation in response to DNA damage stress induced by etoposide (ETOP) in tumor cells...This effect may explain the poorer prognosis observed in breast cancer patients with high expression levels of SIRT5 or MTHFD2. These systematic analyses provide new insights into targeting succinylation-modified metabolic proteins to enhance TIS, and their combination with senolytics for breast cancer therapy.

By integrating metabolic regulation with disease mechanisms, Kmal has emerged as a crucial biochemical modification with broad implications for metabolic, inflammatory, and oncological disorders. Understanding its regulatory network will be pivotal in developing precision medicine approaches aimed at mitigating disease progression and restoring cellular homeostasis.