The yin and yang faces of the mitochondrial deacetylase sirtuin 3 in age-related disorders.

The yin and yang faces of the mitochondrial deacetylase sirtuin 3 in age-related disorders. Ageing Res Rev. 2019 Nov 15;:100983 Authors: Gomes P, Viana SD, Nunes S, Rolo AP, Palmeira CM, Reis F Abstract Aging, the most important risk factor for many of the chronic diseases affecting Western society, is associated with a decline in mitochondrial function and dynamics. Sirtuin 3 (SIRT3) is a mitochondrial deacetylase that has emerged as a key regulator of fundamental processes which are frequently dysregulated in aging and related disorders. This review highlights recent advances and controversies regarding the roles of SIRT3 in metabolic, cardiovascular and neurodegenerative diseases, as well as the use of SIRT3 modulators as a therapeutic strategy against those disorders. Although most studies point to a protective role upon SIRT3 activation, there are conflicting findings that need a better elucidation. The discovery of novel SIRT3 modulators with higher selectivity together with the assessment of the relative importance of different SIRT3 enzymatic activities and the relevance of crosstalk between distinct sirtuin isoforms will be pivotal to validate SIRT3 as a useful drug target for the prevention and treatment of age-related diseases. PMID: 31740222 [PubMed - as supplied by publisher]
Source: Ageing Research Reviews - Category: Genetics & Stem Cells Authors: Tags: Ageing Res Rev Source Type: research

Related Links:

In conclusion, SMI prevents DOX-induced cardiotoxicity, inhibits mitochondrial oxidative stress and mitochondrial fragmentation through activation of AMPK and PI3K/Akt/GSK-3β signaling pathway.
Source: Frontiers in Pharmacology - Category: Drugs & Pharmacology Source Type: research
Mitochondrial dysfunction is implicated in sporadic and familial Parkinson's disease (PD). However, the mechanisms that impair homeostatic responses to mitochondrial dysfunction remain unclear. Previously, we found that chronic, low-dose administration of the mitochondrial complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+) dysregulates mitochondrial fission–fusion, mitophagy, and mitochondrial biogenesis. Given that PTEN-induced kinase 1 (PINK1) regulates mitochondrial function, dynamics, and turnover, we hypothesized that alterations in endogenous PINK1 levels contribute to depletion of mitochondria during chron...
Source: Journal of Biological Chemistry - Category: Chemistry Authors: Tags: Molecular Bases of Disease Source Type: research
Conclusion: The sequence alignments of the isolates displayed two profiles. All sequenced samples showed E. granulosus sensu stricto (G1) with no organ-related genotype. PMID: 32489385 [PubMed]
Source: Iranian Journal of Parasitology - Category: Parasitology Tags: Iran J Parasitol Source Type: research
Publication date: September 2020Source: Molecular Genetics and Metabolism Reports, Volume 24Author(s): Mohammed A. Almuqbil, Hilary J. Vernon, Marcia Ferguson, Antonie D. Kline
Source: Molecular Genetics and Metabolism Reports - Category: Genetics & Stem Cells Source Type: research
Abstract The imbalance between increased oxidative agents and antioxidant defence mechanisms is central in the pathogenesis of obstructive lung diseases such as asthma and COPD. In these patients, there are increased levels of reactive oxygen species. Superoxide anions (O2 - ), hydrogen peroxide (H2O2) and hydroxyl radicals (.OH) are critical for the formation of further cytotoxic radicals in the bronchi and lung parenchyma. Chronic inflammation, partly induced by oxidative stress, can further increase the oxidant burden through activated phagocytic cells (neutrophils, eosinophils, macrophages), particularly in se...
Source: Current Medicinal Chemistry - Category: Chemistry Authors: Tags: Curr Med Chem Source Type: research
In today's open access paper, the authors survey the work of the past decade in the use of proteomics to assess the consequences of cellular senescence. Senescent cells accumulate with age, but even in late age they remain a tiny fraction of all cells. The harms caused by the long-term presence of senescent cells occur because these cells secrete a potent mix of inflammatory signals, growth factors, and other molecules that rouse the immune system, promote fibrosis and other dysfunctions in tissue maintenance, encourage other cells to also become senescent, and so forth. This senescence-associated secretory phenotype is ac...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs
In conclusion, our study proposes a potential therapy strategy for the incurable ABP. PMID: 32475920 [PubMed - in process]
Source: Biological and Pharmaceutical Bulletin - Category: Drugs & Pharmacology Authors: Tags: Biol Pharm Bull Source Type: research
Autophagy is the name given to a collection of processes responsible for recycling damaged or otherwise unwanted structures and proteins in the cell. With age, autophagy becomes less efficient. Many individual mechanisms falter, and the end result is that cells become more cluttered with damaged parts and harmful proteins. Scaled up across entire organs, this has a meaningful contribution to the progression of aging and age-related disease. Interestingly, increased or more efficient autophagy appears to be a centrally important mechanism in the benefits to health and longevity provided by calorie restriction and a range of...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs
Evidence strongly suggests that the global faltering of mitochondrial function throughout the body with advancing age has a lot to do with a decline in the effectiveness of mitophagy. Mitochondria are the power plants of the cell, a herd of hundreds swarming and replicating like bacteria in every cell to produce the chemical energy store molecule ATP. Mitophagy is the specialized form of autophagy that destroys worn and damaged mitochondria, recycling their component parts. Without it, cells would become overtaken by broken, malfunctioning mitochondria. Mitochondrial dysfunction leads to too little ATP, but also higher lev...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs
Abstract Initially discovered as a protease responsible for degradation of misfolded or damaged proteins, the mitochondrial Lon protease (Lonp1) turned out to be a multifaceted enzyme, that displays at least three different functions (proteolysis, chaperone activity, binding of mtDNA) and that finely regulates several cellular processes, within and without mitochondria. Indeed, LONP1 in humans is ubiquitously expressed, and is involved in regulation of response to oxidative stress and, heat shock, in the maintenance of mtDNA, in the regulation of mitophagy. Furthermore, its proteolytic activity can regulate severa...
Source: International Review of Cell and Molecular Biology - Category: Cytology Authors: Tags: Int Rev Cell Mol Biol Source Type: research
More News: Brain | Cardiology | Cardiovascular | Genetics | Heart | Mitochondrial Disease | Neurology | Neuroscience | Science | Study