scholarly journals Interplay Between Mitochondrial Proteins and Age-Associated Risk of Cardiovascular Diseases

2018 ◽  
Author(s):  
Zuzana Tatarkova ◽  
Martin Kolisek ◽  
Ivana Pilchova ◽  
Peter Racay ◽  
Peter Kaplan
Keyword(s):  
Cardiovascular Diseases ◽  
Mitochondrial Proteins

Mitochondria-Associated Proteostasis

2020 ◽  
Vol 49 (1) ◽  
pp. 41-67 ◽  
Author(s):  
Linhao Ruan ◽  
Yuhao Wang ◽  
Xi Zhang ◽  
Alexis Tomaszewski ◽  
Joshua T. McNamara ◽  
...  
Keyword(s):  
Quality Control ◽  
Cardiovascular Diseases ◽  
Protein Quality ◽  
Therapeutic Potential ◽  
Nuclear Genome ◽  
Mitochondrial Proteins ◽  
Protein Homeostasis ◽  
Control Mechanisms ◽  
Mitochondrial Proteome ◽  
Functional States

Mitochondria are essential organelles in eukaryotes. Most mitochondrial proteins are encoded by the nuclear genome and translated in the cytosol. Nuclear-encoded mitochondrial proteins need to be imported, processed, folded, and assembled into their functional states. To maintain protein homeostasis (proteostasis), mitochondria are equipped with a distinct set of quality control machineries. Deficiencies in such systems lead to mitochondrial dysfunction, which is a hallmark of aging and many human diseases, such as neurodegenerative diseases, cardiovascular diseases, and cancer. In this review, we discuss the unique challenges and solutions of proteostasis in mitochondria. The import machinery coordinates with mitochondrial proteases and chaperones to maintain the mitochondrial proteome. Moreover, mitochondrial proteostasis depends on cytosolic protein quality control mechanisms during crises. In turn, mitochondria facilitate cytosolic proteostasis. Increasing evidence suggests that enhancing mitochondrial proteostasis may hold therapeutic potential to protect against protein aggregation–associated cellular defects.

scholarly journals The Role of Mitochondrial DNA Mutations in Cardiovascular Diseases

2022 ◽  
Vol 23 (2) ◽  
pp. 952
Author(s):  
Siarhei A. Dabravolski ◽  
Victoria A. Khotina ◽  
Vasily N. Sukhorukov ◽  
Vladislav A. Kalmykov ◽  
Liudmila M. Mikhaleva ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Mitochondrial Proteins ◽  
Mitochondrial Trna ◽  
Mtdna Mutations ◽  
Mitochondrial Dna Mutations ◽  
Dna Mutations ◽  
Artery Disease

Cardiovascular diseases (CVD) are one of the leading causes of morbidity and mortality worldwide. mtDNA (mitochondrial DNA) mutations are known to participate in the development and progression of some CVD. Moreover, specific types of mitochondria-mediated CVD have been discovered, such as MIEH (maternally inherited essential hypertension) and maternally inherited CHD (coronary heart disease). Maternally inherited mitochondrial CVD is caused by certain mutations in the mtDNA, which encode structural mitochondrial proteins and mitochondrial tRNA. In this review, we focus on recently identified mtDNA mutations associated with CVD (coronary artery disease and hypertension). Additionally, new data suggest the role of mtDNA mutations in Brugada syndrome and ischemic stroke, which before were considered only as a result of mutations in nuclear genes. Moreover, we discuss the molecular mechanisms of mtDNA involvement in the development of the disease.

scholarly journals Natural Bioactive Compounds As Protectors Of Mitochondrial Dysfunction In Cardiovascular Diseases And Aging

Molecules ◽  
2019 ◽  
Vol 24 (23) ◽  
pp. 4259 ◽  
Author(s):  
Diego Arauna ◽  
María Furrianca ◽  
Yolanda Espinosa-Parrilla ◽  
Eduardo Fuentes ◽  
Marcelo Alarcón ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Bioactive Compounds ◽  
Healthy Aging ◽  
Functional Foods ◽  
Protective Factor ◽  
Mitochondrial Proteins ◽  
Oxygen Species ◽  
Cellular Mechanisms ◽  
Potential Use

Diet, particularly the Mediterranean diet, has been considered as a protective factor against the development of cardiovascular diseases, the main cause of death in the world. Aging is one of the major risk factors for cardiovascular diseases, which have an oxidative pathophysiological component, being the mitochondria one of the key organelles in the regulation of oxidative stress. Certain natural bioactive compounds have the ability to regulate oxidative phosphorylation, the production of reactive oxygen species and the expression of mitochondrial proteins; but their efficacy within the mitochondrial physiopathology of cardiovascular diseases has not been clarified yet. The following review has the purpose of evaluating several natural compounds with evidence of mitochondrial effect in cardiovascular disease models, ascertaining the main cellular mechanisms and their potential use as functional foods for prevention of cardiovascular disease and healthy aging.

Inflammageing in the cardiovascular system: mechanisms, emerging targets, and novel therapeutic strategies

2020 ◽  
Vol 134 (17) ◽  
pp. 2243-2262
Author(s):  
Danlin Liu ◽  
Gavin Richardson ◽  
Fehmi M. Benli ◽  
Catherine Park ◽  
João V. de Souza ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Cardiovascular Research ◽  
Inflammatory Processes ◽  
Ach Receptors

Abstract In the elderly population, pathological inflammation has been associated with ageing-associated diseases. The term ‘inflammageing’, which was used for the first time by Franceschi and co-workers in 2000, is associated with the chronic, low-grade, subclinical inflammatory processes coupled to biological ageing. The source of these inflammatory processes is debated. The senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammageing. The SASP is characterised by the release of inflammatory cytokines, elevated activation of the NLRP3 inflammasome, altered regulation of acetylcholine (ACh) nicotinic receptors, and abnormal NAD+ metabolism. Therefore, SASP may be ‘druggable’ by small molecule therapeutics targeting those emerging molecular targets. It has been shown that inflammageing is a hallmark of various cardiovascular diseases, including atherosclerosis, hypertension, and adverse cardiac remodelling. Therefore, the pathomechanism involving SASP activation via the NLRP3 inflammasome; modulation of NLRP3 via α7 nicotinic ACh receptors; and modulation by senolytics targeting other proteins have gained a lot of interest within cardiovascular research and drug development communities. In this review, which offers a unique view from both clinical and preclinical target-based drug discovery perspectives, we have focused on cardiovascular inflammageing and its molecular mechanisms. We have outlined the mechanistic links between inflammageing, SASP, interleukin (IL)-1β, NLRP3 inflammasome, nicotinic ACh receptors, and molecular targets of senolytic drugs in the context of cardiovascular diseases. We have addressed the ‘druggability’ of NLRP3 and nicotinic α7 receptors by small molecules, as these proteins represent novel and exciting targets for therapeutic interventions targeting inflammageing in the cardiovascular system and beyond.

Self-efficacy and quality of life among people with cardiovascular diseases: A meta-analysis.

2018 ◽  
Vol 63 (2) ◽  
pp. 295-312 ◽  
Author(s):  
Anna Banik ◽  
Ralf Schwarzer ◽  
Nina Knoll ◽  
Katarzyna Czekierda ◽  
Aleksandra Luszczynska
Keyword(s):  
Quality Of Life ◽  
Cardiovascular Diseases ◽  
Self Efficacy ◽  
Meta Analysis

Apolipoprotein(a), Fibrinopeptide A and Carotid Atherosclerosis in Middle-Aged Men

1994 ◽  
Vol 72 (04) ◽  
pp. 563-566 ◽  
Author(s):  
Tuomo Rankinen ◽  
Sari Väisänen ◽  
Michele Mercuri ◽  
Rainer Rauramaa
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Carotid Atherosclerosis ◽  
Intima Media Thickness ◽  
Carotid Bifurcation ◽  
Carotid Intima Media Thickness ◽  
Fibrinopeptide A ◽  
Carotid Imt ◽  
Apolipoprotein A ◽  
The Difference

SummaryThe association between apolipoprotein(a) [apo(a)], fibrinogen, fibrinopeptide A (FPA) and carotid intima-media thickness (IMT) was analyzed in Eastern Finnish men aged 50 to 60 years. Apo(a) correlated directly with carotid bifurcation (r = 0.26, p = 0.001), but not with common carotid IMT. Men in the lowest quartile of apo(a) had thinner (p = 0.013) IMT in bifurcation [1.59 mm (95% Cl 1.49; 1.68)] compared to the men in the highest [1.91 mm (95% Cl 1.73; 2.09)] apo(a) quartile. The difference remained (p=0.038) after adjusting for confounders. Plasma fibrinogen was not related to carotid IMT, whereas FPA correlated with common carotid (r = 0.21, p = 0.016) and carotid bifurcation (r = 0.21, p = 0.018) IMT. These associations abolished after adjusting for the confounders. The data suggest that apo(a) associate with carotid atherosclerosis independent of other risk factors for ischemic cardiovascular diseases.

Sign in / Sign up

Export Citation Format

Share Document