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Renal Fibrosis: SIRT1 Still of Value
Huailiang Wu1, Zhen Qiu1, Liyan Wang2
1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Abstract:
Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
Insights
Sirtuin 1 (SIRT1) plays a complex role in kidney fibrosis, impacting processes like aging and inflammation. Understanding SIRT1 mechanisms may reveal new therapeutic targets for chronic kidney disease (CKD) treatment.
Area of Science:
- Nephrology
- Molecular Biology
- Biochemistry
Background:
- Chronic kidney disease (CKD) is a significant global health issue, with renal fibrosis being a common pathway to end-stage renal disease.
- Current treatments for renal fibrosis are limited, highlighting the need for novel therapeutic strategies.
- Sirtuin 1 (SIRT1), a NAD+-dependent deacetylase, is involved in kidney physiology and pathology, but its precise role in renal fibrosis remains debated.
Purpose of the Study:
- To comprehensively review the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression.
- To explore the potential of SIRT1 as a therapeutic target for mitigating renal fibrosis.
- To offer new perspectives on treatment approaches and prognostic assessments for CKD.
Main Methods:
- Literature review synthesizing current research on SIRT1 and renal fibrosis.
- Analysis of SIRT1's involvement in key fibrotic pathways including lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy.
- Evaluation of existing evidence regarding SIRT1's protective or detrimental effects in renal fibrosis models.
Main Results:
- SIRT1 influences multiple cellular processes implicated in renal fibrosis, such as oxidative stress, inflammation, and autophagy.
- Contradictory findings exist regarding SIRT1's exact role, suggesting context-dependent effects.
- Evidence points to SIRT1's potential in modulating fibrotic progression through various molecular mechanisms.
Conclusions:
- SIRT1 is a critical regulator in the complex pathogenesis of renal fibrosis.
- Targeting SIRT1 pathways presents a promising avenue for developing novel therapeutic interventions for CKD.
- Further research is warranted to elucidate the precise mechanisms and optimize SIRT1-based strategies for renal fibrosis treatment.
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