Influence of mitochondrion-toxic agents on the cardiovascular system

Finsterer, Josef; Ohnsorge, Peter

doi:10.1016/j.yrtph.2013.09.002

Cited by 74 publications

(55 citation statements)

References 108 publications

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“…Doxorubicin is notable because it prevents expression of compensatory mitochondrial biogenesis (Suliman et al, 2007a;Finsterer and Ohnsorge, 2013). Certain antibiotics (e.g., tetracycline and aminoglycosides) inhibit mtDNA translation and protein synthesis.…”

Section: Mitochondrial Dysfunction Caused By Therapeutic Agentsmentioning

confidence: 99%

Mitochondrial Quality Control as a Therapeutic Target

2015

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Section: Mitochondrial Dysfunction Caused By Therapeutic Agentsmentioning

confidence: 99%

Mitochondrial Quality Control as a Therapeutic Target

2015

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“…Unlike tanshinone I and tanshinone IIA, fewer studies of cryptotanshinone have been focused on the pharmacological effects including the cardiovascular protection. Research indicates ADRinduced cardiotoxicity via mitochondria (Carvalho et al, 2014;Finsterer & Ohnsorge, 2013). Given that CRY can adjust the oxidative stress (Chen et al, 2014), which is caused by mitochondria, this research mainly focused on the protection on cardiomyocytes via mitochondria instead of other organelles.…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone protects against adriamycin-induced mitochondrial dysfunction in cardiomyocytes

Zhang

Chen

et al. 2015

Pharmaceutical Biology

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Results: 50 mg/kg CRY significantly promoted the energy production of ATP (16.99 ± 2.38 nmol/g Pro) (Pro: Protein) by increasing the complexes activities except II (p40.05). After the treatment of CRY, the suppressed MMP was increased while superoxide anion free radical (0.57 ± 0.07/mg Pro) was inhibited markedly. Mitochondrial biogenesis-relative factors PGC-1a, NRF-1, and TFAM were also promoted. Remarkable augmentations of NO, inducible nitric oxide synthase (iNOS), and increased activity of GSH-PX (p50.05) were also detected after the treatment of CRY, while no obvious changes on the activity of nitric oxide synthase (cNOS; p40.05) were observed. Discussion and conclusion: These results suggest that CRY protects against ADR-induced mitochondrial dysfunction in cardiomyocytes. It could be an ideal potential drug of cardioprotection.

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“…Mitochondrial toxicity can lead to higher levels of markers of endothelial dysfunction and target end organ damage. Mitochondrial toxicity can also directly alter BP and lead to a number of risk factors associated with high BP, such as arrhythmia [61,62]. ART initiation has also been associated with changes in body composition including excess weight gain and lipodystrophy, which both are associated with increased hypertension risk [1••, 51, 52].…”

Section: Inflammationmentioning

confidence: 99%

Mechanisms Influencing Circadian Blood Pressure Patterns Among Individuals with HIV

et al. 2015

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HIV+ individuals have an increased risk for cardiovascular disease (CVD), but the mechanisms behind this association are poorly understood. While hypertension is a well-established CVD risk factor, clinic-based blood pressure (BP) assessment by itself cannot identify several important BP patterns, including white coat hypertension, masked hypertension, nighttime hypertension, and nighttime BP dipping. These BP patterns can be identified over a 24-h period by ambulatory BP monitoring (ABPM). In this review, we provide an overview of the potential value of conducting ABPM in HIV+ individuals. ABPM phenotypes associated with increased CVD risk include masked hypertension (i.e., elevated out-of-clinic BP despite non-elevated clinic BP), nighttime hypertension, and a non-dipping BP pattern (i.e., a drop in BP of <10 % from daytime to nighttime). These adverse ABPM phenotypes may be highly relevant in the setting of HIV infection, given that increased levels of inflammatory biomarkers, high psychosocial burden, high prevalence of sleep disturbance, and autonomic dysfunction have been commonly reported in HIV+ persons. Additionally, although antiretroviral therapy (ART) is associated with lower AIDS-related morbidity and CVD risk, the mitochondrial toxicity, oxidative stress, lipodystrophy, and insulin resistance associated with long-term ART use potentially lead to adverse ABPM phenotypes. Existing data on ABPM phenotypes in the setting of HIV are limited, but suggest an increased prevalence of a non-dipping BP pattern. In conclusion, identifying ABPM phenotypes may provide crucial information regarding the mechanisms underlying the excess CVD risk in HIV+ individuals.

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Influence of mitochondrion-toxic agents on the cardiovascular system

Cited by 74 publications

References 108 publications

Mitochondrial Quality Control as a Therapeutic Target

Mitochondrial Quality Control as a Therapeutic Target

Cryptotanshinone protects against adriamycin-induced mitochondrial dysfunction in cardiomyocytes

Mechanisms Influencing Circadian Blood Pressure Patterns Among Individuals with HIV

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