Sirtuins as Novel Biological Targets for Pharmacological Intervention in Physiology and Pathology—2nd Edition

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 633

Special Issue Editors


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Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, viale Regina Elena 324, 00161 Rome, Italy
Interests: sirtuins; metabolism; extracellular vesicles; autophagy; mitophagy; apoptosis
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Special Issue Information

Dear Colleagues,

The sirtuin family of proteins is a class of enzymes that is highly conserved from yeast to humans, possessing a high homology in their sequences and cellular functions, underlying the fact that these proteins play important physiological roles. Seven mammalian sirtuins have been identified, which are characterized by different cellular functions, structures and localizations that can vary based on different stimuli. Sirtuins were first characterized as histone deacetylases, but the presence of non-histone targets underline their involvement in many cellular processes such as the cell cycle, differentiation, senescence, stress response, inflammation, aging, and metabolism. On the other hand, sirtuins are involved in several pathological conditions, such as neurodegenerative disorders, cardiovascular diseases, metabolism-related disorders, carcinogenesis, and tumor development, in which they can act as disease promoters or protective factors based on their targets and functions. Nuclear sirtuins, due to their epigenetic role, and mitochondrial sirtuins, due to their involvement in several metabolic processes, such as the tricarboxylic acid cycle, respiratory chain, fatty acid β-oxidation, ketogenesis, glutamine metabolism, etc., represent an important object of investigation hallmarks of carcinogenesis, represented by metabolic reprogramming and uncontrolled cell proliferation. In a broader analysis that also considers the influence of sirtuins in physiological and pathological conditions, this class of proteins represents a promising potential target of molecular and pharmacological strategies that could counteract the effects of several pathological conditions acting at various levels in molecular and cellular mechanisms. This Special Issue aims to collect and summarize the latest findings on the potential of sirtuin-based pharmacological interventions to modulate activity and counteract damage and the onset of pathological states, favoring the physiological homeostasis of tissues.

Dr. Michele Aventaggiato
Dr. Marco Tafani
Guest Editors

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Keywords

  • sirtuins
  • metabolism
  • cancer
  • hypoxia
  • damage recovery
  • cell death

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Published Papers (1 paper)

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Research

26 pages, 5270 KiB  
Article
Gallic Acid and Taurine Attenuate Thiamethoxam-Induced Hepatotoxicity in Rats by Modulating SIRT-1/PGC-1α, NF-κB/iNOS, and p53/Bax/Caspase-3 Pathways
by Sara T. Elazab, Fatmah A. Safhi, Rasha K. Al-Akeel, Raghda H. Deraz, Souvarish Sarkar and Rania Essam Ali Gamal Eldin
Pharmaceuticals 2025, 18(8), 1112; https://doi.org/10.3390/ph18081112 - 25 Jul 2025
Viewed by 452
Abstract
Background/Objectives: Thiamethoxam (TMX) is one of the most extensively utilized insecticides of the neonicotinoid family; however, its application is associated with notable toxic effects on multiple organs of mammals. Our purpose was to explore the potential hepatoprotective effect of taurine (TAU) and/or [...] Read more.
Background/Objectives: Thiamethoxam (TMX) is one of the most extensively utilized insecticides of the neonicotinoid family; however, its application is associated with notable toxic effects on multiple organs of mammals. Our purpose was to explore the potential hepatoprotective effect of taurine (TAU) and/or gallic acid (GA) against TMX-induced liver damage, with an emphasis on their role in regulating SIRT-1/PGC-1α, NF-κB/iNOS, and p53/Bax/caspase-3 pathways. Methods: Rats were assigned to seven groups (n = 6) and gavaged daily for 28 days with saline (control group), TAU at 50 mg/kg, GA at 20 mg/kg, TMX at 78.15 mg/kg, TMX + TAU, TMX + GA, and TMX + TAU + GA. Results: The findings revealed that TAU and/or GA attenuated TMX-induced liver injury, as demonstrated by the restoration of hepatic performance hallmarks and histological structure. TAU and GA mitigated TMX-mediated oxidative stress and boosted the antioxidant defense mechanism by upregulating the transcription levels of SIRT-1, PGC-1α, Nrf2, and HO-1. Moreover, TAU and GA suppressed TMX-associated inflammatory response by increasing IL-10 concentration and lowering the levels of NF-κB, IL-1β, and iNOS; the mRNA levels of NLRP3; and TNF-α immunoexpression. Both compounds, individually or concurrently, exerted an anti-apoptotic effect in TMX-treated rats, evidenced by increased Bcl-2 expression and reduced p53 mRNA level, Bax expression, and caspase-3 concentration. Conclusions: TAU and/or GA may be regarded as promising remedies that can alleviate TMX-induced hepatotoxicity by activating SIRT-1/PGC-1α signaling and abolishing inflammation and apoptosis. Full article
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