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Genetics and exercise: an introduction
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Claude Bouchard, Henning Wackerhage
You probably wonder about the 5’ and 3’ ends, and the “AAA” annotation at the end of the mRNA sequence. The 5’ and 3’ refer to the position of specific carbon atoms in the deoxyribose sugar of a DNA strand and provide information about the direction of the DNA strand. The “AAA” symbolizes the so-called poly-A tail added to each mRNA after transcription, which makes RNA more stable. Transcription of RNA takes place in the nucleus of the cell, whilst translation of proteins in the ribosomes occur in the cytoplasm. Once translated into a polypeptide, posttranslational modifications such as phosphorylation, methylation or acetylation may happen to generate a mature, functional protein or change how active the protein is.
Ruptured Abdominal Aortic Aneurysms
Published in Stephen M. Cohn, Peter Rhee, 50 Landmark Papers, 2019
Abdul Q. Alarhayem, Mark G. Davies
Abdominal aortic aneurysms (AAA) affect 7%–9% of the population over the age of 65 years, with a higher prevalence in smokers. The natural course of an unrepaired AAA is continued growth, and ultimately rupture and death. Aneurysm diameter, expansion rate, female gender, low FEV1, current smoking, and hypertension have all been associated with an increased risk of rupture.
Regulation of Antiviral Immunity by Mitochondrial Dynamics
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Mohsin Khan, Hasan Imam, Saiful Anam Mir
Post-translational modifications and proteolysis of OPA1 and Mfns are well reported (Khan et al., 2015). Because of differential RNA splicing, OPA1 exists as distinct isoforms (Baker et al., 2014; Ehses et al., 2009; Head et al., 2009). The longer isoform of OPA1 contains membrane anchor. Although, the short isoform lacks membrane anchor it can interact with membrane proteins. Both long and short OPA1 isoforms can impel IMM fusion, however under stress condition only the long isoform promotes mitochondrial fusion. SIRT1-mediated deacetylation can regulate the activity of OPA1 (Samant et al., 2014). Reduction in mitochondrial membrane potential triggers the proteolysis of OPA1 by OMA1 (Overlapping with the M-AAA Protease 1 Homolog) (Baker et al., 2014; Ehses et al., 2009). Under normal cellular condition OMA1 is constitutively active. Various stress stimulation can increase its catalytic activity several fold. Study by Baker et al, identified a stress sensor N-terminal domain of OMA1, which is responsible for its stress-induced activation (Baker et al., 2014).
Proteomics applications in biomarker discovery and pathogenesis for abdominal aortic aneurysm
Published in Expert Review of Proteomics, 2021
Jianqiang Wu, Wei Wang, Zhaoran Chen, Fang Xu, Yuehong Zheng
The development of AAA is a complex pathophysiological process. Currently, the pathogenesis of AAA is not fully understood. The known pathological features of AAA involve infiltration of the aortic wall by inflammatory and immune cells, degradation of the extracellular matrix by proteases, loss of vascular smooth muscle cells (SMCs) in the media, formation of an intraluminal thrombus (ILT), neovascularization, and oxidative stress [10–13]. Currently, no specific drug treatments can limit the growth or rupture risk of AAA [14]. The only available treatment for AAA is open or endovascular surgical repair, which is usually suitable for large AAAs (diameter >5.5 cm) or those with diameter increases >1 cm per year [15–17]. AAA is usually asymptomatic and frequently diagnosed during occasional imaging examinations in developing countries. Besides, AAA can be detected by ultrasonography screening at the age of more than 65, conducted in several developed countries [18,19]. The AAA diameter is strongly correlated with the risk of rupture, with a larger diameter associated with a higher risk of rupture [20]. However, AAA diameter as a surgical or prognostic indicator is also controversial because small aneurysms can sometimes rupture, and large aneurysms may remain stable for a very long time [21,22]. Therefore, it is essential to explore the pathogenesis of AAA and identify early diagnostic biomarkers, prognostic biomarkers, and potential therapeutic targets for the current management of AAA.
Alzheimer’s Disease and Parkinson’s Disease: A Nutritional Toxicology Perspective of the Impact of Oxidative Stress, Mitochondrial Dysfunction, Nutrigenomics and Environmental Chemicals
Published in Journal of the American College of Nutrition, 2020
Aayushi Agnihotri, Okezie I. Aruoma
Mitochondria play important roles in cell respiratory processes, metabolism, energy production, intracellular signaling, free radical production, and apoptosis. In neurodegenerative diseases, mitochondrial dysfunction is associated with a compromised energy production, impaired calcium buffering, activation of proteases and phospholipases, and increased oxidative stress (6–8). Increased level of oxidative stress and accumulation of mitochondrial DNA mutations resulting in mitochondrial dysfunction plays an important role in the aging process and the pathogenesis of many neurodegenerative diseases (9,10). Impaired calcium influx, dissipation of mitochondrial membrane potential, accumulation of mutant proteins in mitochondria, increased accumulation of mtDNA deficiencies, and deficiencies in mitochondrial oxidative phosphorylation are significant cellular changes in late‐onset neurodegenerative diseases (11). Reference (12) suggested that mitochondrial proteases in the inner membrane perform the quality control surveillance by having chaperone-like activities and degrading the misfolded proteins and play a crucial role in the pathogenesis of many neurodegenerative diseases. The m-AAA protease is a key modulator of mitochondrial quality control system. Loss of m-AAA protease promotes neurodegeneration through various pathways, including decreased mitochondrial protein synthesis due to impaired maturation of Mrpl32, accumulation of misfolded proteins, defective Opa1-mediated mitochondrial fusion, abnormal mitochondrial transport and reduced assembly and stability of complexes I and III (12).
Nationwide survey of 199 patients with reactive amyloid a amyloidosis in Japan
Published in Amyloid, 2019
Yasuaki Okuda, Toshiyuki Yamada, Mitsuharu Ueda, Yukio Ando
A total of 199 patients with AAA were included in the present study. The underlying diseases of AAA were rheumatoid arthritis (60.3%), uncharacterized inflammatory disorders (11.1%), neoplasms (7.0%), other rheumatic diseases (6.5%), inflammatory bowel diseases (4.5%), chronic infection (4.5%), Castleman’s disease (4.0%), and autoinflammatory diseases (2.0%). The clinical manifestations at the diagnosis of AAA were moderate to severe renal dysfunction (46.2%), moderate to severe proteinuria (30.7%), intractable diarrhea (32.2%), melena (4.5%), paralytic ileus (3.5%), heart failure (11.6%), cardiac conduction disturbances (10.1%), arrhythmia (5.5%), and hypothyroidism (11.6%). Diagnostic biopsies were performed most frequently in the gastrointestinal tract (66.3%), followed by the kidneys (22.1%), heart (5.5%), abdominal fat (4.0%), and others (3.0%). Biologics were used to treat 97 patients with AA amyloidosis (48.7%). Tocilizumab (TCZ) was administered to 66 patients, with 95.5% showing good responses. Anti-TNF agents were administered to 27 patients, with 74.1% showing good responses. The treatment effects of TCZ were significantly superior to those of anti-TNF agents (p < .007).