Targeting Mitochondria in Cardiovascular Diseases

Silva, Filomena S. G.; Simões, Rui F.; Couto, Renata; Oliveira, Paulo J.

doi:10.2174/1381612822666160822150243

Cited by 33 publications

(17 citation statements)

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“…As dysfunctional mitochondria contribute to increased ROS production, they may be suitable targets for bioactive compounds with antioxidant properties. Indeed, dietary antioxidants, such as vitamin C, polyunsaturated fatty acids (PUFA), quercetin, resveratrol and curcumin, may reduce mitochondrial oxidative damage . Although it is conceivable that these nutrients may improve mitochondrial function in CKD, only a few experimental studies have been conducted so far.…”

Section: Nutritional Strategies Targeting Mitochondrial Dysfunction Imentioning

confidence: 99%

“…Indeed, dietary antioxidants, such as vitamin C, polyunsaturated fatty acids (PUFA), quercetin, resveratrol and curcumin, may reduce mitochondrial oxidative damage. [55][56][57] Although it is conceivable that these nutrients may improve mitochondrial function in CKD, only a few experimental studies have been conducted so far. In this review, we have searched the literature on therapeutic approaches using bioactive compounds to enhance mitochondrial function and their role in the prevention of uraemic complications, see Figure 2.…”

Section: Targeting Mitochondrial Dysfunction In Ckdmentioning

confidence: 99%

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Bioactive food and exercise in chronic kidney disease: Targeting the mitochondria

Mafra

Gidlund

Borges

et al. 2018

Eur J Clin Investigation

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Chronic kidney disease (CKD), which affects 10%-15% of the population, associates with a range of complications-such as cardiovascular disease, frailty, infections, muscle and bone disorders and premature ageing-that could be related to alterations of mitochondrial number, distribution, structure and function. As mitochondrial biogenesis, bioenergetics and the dynamic mitochondrial networks directly or indirectly regulate numerous intra-and extracellular functions, the mitochondria have emerged as an important target for interventions aiming at preventing or improving the treatment of complications in CKD. In this review, we discuss the possible role of bioactive food compounds and exercise in the modulation of the disturbed mitochondrial function in a uraemic milieu.

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Section: Nutritional Strategies Targeting Mitochondrial Dysfunction Imentioning

confidence: 99%

Section: Targeting Mitochondrial Dysfunction In Ckdmentioning

confidence: 99%

Bioactive food and exercise in chronic kidney disease: Targeting the mitochondria

Mafra

Gidlund

Borges

et al. 2018

Eur J Clin Investigation

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“…Indeed, in 3 large prospective studies mtDNA copy number has been independently associated with CVD incidence, suggesting a potential clinical utility in improving CVD risk classification by this marker [71]. Despite therapies targeting mitochondria in the context of CVDs are not under widespread clinical use, there is a growing interest toward new strategies involving mitochondrial biology in early prevention or treatment of CVD [72].…”

Section: Discussionmentioning

confidence: 99%

A Pilot Study on the Effects of l-Carnitine and Trimethylamine-N-Oxide on Platelet Mitochondrial DNA Methylation and CVD Biomarkers in Aged Women

Bordoni

Sawicka

Szarmach

et al. 2020

IJMS

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l-carnitine supplementation has been used for cardiovascular health protection for a long time. Recently, trimethylamine-N-oxide (TMAO), which is an end product of l-carnitine metabolism via the activity of microbiota, has been identified as a cardiovascular disease (CVD) biomarker. The aim of this study was to assess the effect of 6 months of l-carnitine supplementation in a group of aged women engaged in a regular physical training. Platelet mitochondrial DNA methylation, an emerging and innovative biomarker, lipid profile and TMAO levels have been measured. TMAO increased after l-carnitine supplementation (before 344.3 ± 129.8 ng/mL vs. after 2216.8 ± 1869.0 ng/mL; n = 9; paired t-test, p = 0.02). No significant effects on TMAO were exerted by training alone (n = 9) or by l-leucine supplementation (n = 12). TMAO levels after 6 months of l-carnitine supplementation were associated with higher low-density lipoprotein-cholesterol (LDL-c) (Spearman Rho = 0.518, p = 0.003) and total cholesterol (TC) (Spearman Rho = 0.407, p = 0.026) levels. l-carnitine supplementation increased D-loop methylation in platelets (+6.63%; paired t-test, p = 0.005). D-loop methylation was not directly correlated to the TMAO augmentation observed in the supplemented group, but its increase inversely correlated with TC (Pearson coefficient = −0.529, p = 0.029) and LDL-c (Pearson coefficient = −0.439, p = 0.048). This evidence supports the hypothesis that the correlation between l-carnitine, TMAO and atherosclerosis might be more complex than already postulated, and the alteration of mitochondrial DNA (mtDNA) methylation in platelets could be involved in the pathogenesis of this multifactorial disease.

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“…Different factors could explain the variability of carvedilol efficacy in studies. At a mechanistic level, if the cardioprotection was hypothetically given only due to an antioxidant non-specific mechanism [33], a greater individual variability response could be expected than if the effect were a product of a specific β-blocking interaction. At a methodological level, study weaknesses, such as being observational, open-labeled, single-blind, combining cardiovascular drugs, or having a small sample size probably favored mixed results [26,34].…”

Section: Introductionmentioning

confidence: 99%

Prevention of doxorubicin-induced Cardiotoxicity by pharmacological non-hypoxic myocardial preconditioning based on Docosahexaenoic Acid (DHA) and carvedilol direct antioxidant effects: study protocol for a pilot, randomized, double-blind, controlled trial (CarDHA trial)

Carrasco

Ramirez

Nes

et al. 2020

Trials

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Background: Anthracycline-induced cardiotoxicity (AIC), a condition associated with multiple mechanisms of damage, including oxidative stress, has been associated with poor clinical outcomes. Carvedilol, a β-blocker with unique antioxidant properties, emerged as a strategy to prevent AIC, but recent trials question its effectiveness. Some evidence suggests that the antioxidant, not the β-blocker effect, could prevent related cardiotoxicity. However, carvedilol's antioxidant effects are probably not enough to prevent cardiotoxicity manifestations in certain cases. We hypothesize that breast cancer patients taking carvedilol as well as a non-hypoxic myocardial preconditioning based on docosahexaenoic acid (DHA), an enhancer of cardiac endogenous antioxidant capacity, will develop less subclinical cardiotoxicity manifestations than patients randomized to double placebo. Methods/design: We designed a pilot, randomized controlled, two-arm clinical trial with 32 patients to evaluate the effects of non-hypoxic cardiac preconditioning (DHA) plus carvedilol on subclinical cardiotoxicity in breast cancer patients undergoing anthracycline treatment. The trial includes four co-primary endpoints: changes in left ventricular ejection fraction (LVEF) determined by cardiac magnetic resonance (CMR); changes in global longitudinal strain (GLS) determined by two-dimensional echocardiography (ECHO); elevation in serum biomarkers (hs-cTnT and NT-ProBNP); and one electrocardiographic variable (QTc interval). Secondary endpoints include other imaging, biomarkers and the occurrence of major adverse cardiac events during follow-up. The enrollment and follow-up for clinical outcomes is ongoing.

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Targeting Mitochondria in Cardiovascular Diseases

Abstract: Although effective therapies to target mitochondria in the context of CVDs are not under widespread clinical use, the new strategies proposed constitute a real promise for the development of therapies which may effectively prevent CVDs in the near future.

Cited by 33 publications

References 0 publications

Bioactive food and exercise in chronic kidney disease: Targeting the mitochondria

Bioactive food and exercise in chronic kidney disease: Targeting the mitochondria

A Pilot Study on the Effects of l-Carnitine and Trimethylamine-N-Oxide on Platelet Mitochondrial DNA Methylation and CVD Biomarkers in Aged Women

Prevention of doxorubicin-induced Cardiotoxicity by pharmacological non-hypoxic myocardial preconditioning based on Docosahexaenoic Acid (DHA) and carvedilol direct antioxidant effects: study protocol for a pilot, randomized, double-blind, controlled trial (CarDHA trial)

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