Mitochondria and Cardiac Hypertrophy

Facundo, Heberty T.; Brainard, Robert E.; Caldas, Francisco Rodrigo de Lemos; Lucas, Aline Maria Brito

doi:10.1007/978-3-319-55330-6_11

Cited by 54 publications

(36 citation statements)

References 161 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxidative stress-induced redox imbalance in the cardiomyocytes is one of the primary reasons for the development of myocyte hypertrophy [43]. Mitochondria are responsible for the generation of~95% of ATP required by the heart for functioning, cellular signaling, controlled cell death, and generation of ROS such as superoxide anions and hydrogen peroxide [44]. Hence, prolonged cardiac oxidative stress and development of CH is directly associated with mitochondrial dysfunction and the generation of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Application of Zebrafish Model in the Suppression of Drug-Induced Cardiac Hypertrophy by Traditional Indian Medicine Yogendra Ras

et al. 2020

View full text Add to dashboard Cite

Zebrafish is an elegant vertebrate employed to model the pathological etiologies of human maladies such as cardiac diseases. Persistent physiological stresses can induce abnormalities in heart functions such as cardiac hypertrophy (CH), which can lead to morbidity and mortality. In the present study, using zebrafish as a study model, efficacy of the traditional Indian Ayurveda medicine “Yogendra Ras” (YDR) was validated in ameliorating drug-induced cardiac hypertrophy. YDR was prepared using traditionally described methods and composed of nano- and micron-sized metal particles. Elemental composition analysis of YDR showed the presence of mainly Au, Sn, and Hg. Cardiac hypertrophy was induced in the zebrafish following a pretreatment with erythromycin (ERY), and the onset and reconciliation of disease by YDR were determined using a treadmill electrocardiogram, heart anatomy analysis, C-reactive protein release, and platelet aggregation time-analysis. YDR treatment of CH-induced zebrafish showed comparable results with the Standard-of-care drug, verapamil, tested in parallel. Under in-vitro conditions, treatment of isoproterenol (ISP)-stimulated murine cardiomyocytes (H9C2) with YDR resulted in the suppression of drug-stimulated biomarkers of oxidative stress: COX-2, NOX-2, NOX-4, ANF, troponin-I, -T, and cardiolipin. Taken together, zebrafish showed a strong disposition as a model for studying the efficacy of Ayurvedic medicines towards drug-induced cardiopathies. YDR provided strong evidence for its capability in modulating drug-induced CH through the restoration of redox homeostasis and exhibited potential as a viable complementary therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Application of Zebrafish Model in the Suppression of Drug-Induced Cardiac Hypertrophy by Traditional Indian Medicine Yogendra Ras

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Based on previous studies (17)(18)(19)(20)(21), it was hypothesized that PQQ may be protective against Iso-induced cardiac hypertrophy. There are numerous studies on the pathogenesis of cardiac hypertrophy focusing on myocardial pressure overload, myocardial apoptosis, vascular remodeling, oxidative stress and the inflammatory response (4,(22)(23)(24)(25)(26); however, the pathogenesis of cardiac hypertrophy has not yet been fully clarified. The inflammatory response is one of the research hotspots in the pathogenesis of cardiac hypertrophy (26).…”

Section: Pyrroloquinoline Quinone Attenuates Isoproterenol Hydrochlormentioning

confidence: 99%

Pyrroloquinoline quinone attenuates isoproterenol hydrochloride‑induced cardiac hypertrophy in AC16 cells by inhibiting the NF‑κB signaling pathway

et al. 2020

View full text Add to dashboard Cite

Pyrroloquinoline quinone (PQQ) is a naturally occurring redox co-factor that functions as an essential nutrient and antioxidant, and has been reported to exert potent anti-inflammatory effects. However, the therapeutic potential of PQQ for isoproterenol hydrochloride (Iso)-induced cardiac hypertrophy has not yet been explored, at least to the best of our knowledge. In the present study, the anti-inflammatory effects of PQQ were investigated in Iso-treated AC16 cells, a myocardial injury cellular model characterized by an increase in the apparent surface area of the cells and the activation of intracellular cardiac hypertrophy-associated proteins. The results revealed that pre-treatment with PQQ significantly inhibited the expression of cardiac hypertrophy marker proteins, such as atrial natriuretic peptide, brain natriuretic peptide and β-myosin heavy chain. PQQ also inhibited the activation of the nuclear factor (NF)-κB signaling pathway in Iso-treated AC16 cells, thus inhibiting the nuclear translocation of NF-κB and reducing the phosphorylation levels of p65. On the whole, the findings of this study suggest that PQQ may be a promising therapeutic agent for effectively reversing the progression of cardiac hypertrophy.

show abstract

“…Thus, preserving mitochondrial function is integral to protecting cardiac function. Significantly, mitochondrial dysfunction starts to occur in hypertrophy and in the early stages of heart failure making it an attractive therapeutic target for attenuating heart failure progression (Facundo et al, ). Changes to substrate utilization, ion homeostasis and an elevated production of ROS are all mitochondrial abnormalities of heart failure that have been discussed at length elsewhere (and recently reviewed by Brown et al ., ).…”

Section: Mitochondrial Dysfunction Is Linked To Heart Failure Developmentioning

confidence: 99%

Three‐dimensional electron microscopy techniques for unravelling mitochondrial dysfunction in heart failure and identification of new pharmacological targets

Daghistani

Rajab

Kitmitto

2018

British J Pharmacology

View full text Add to dashboard Cite

A hallmark of heart failure is mitochondrial dysfunction leading to a bioenergetics imbalance in the myocardium. Consequently, there is much interest in targeting mitochondrial abnormalities to attenuate the pathogenesis of heart failure. This review discusses (i) how electron microscopy (EM) techniques have been fundamental for the current understanding of mitochondrial structure–function, (ii) the paradigm shift in resolutions now achievable by 3‐D EM techniques due to the introduction of direct detection devices and phase plate technology, and (iii) the application of EM for unravelling mitochondrial pathological remodelling in heart failure. We further consider the tremendous potential of multi‐scale EM techniques for the development of therapeutics, structure‐based ligand design and for delineating how a drug elicits nanostructural effects at the molecular, organelle and cellular levels. In conclusion, 3‐D EM techniques have entered a new era of structural biology and are poised to play a pivotal role in discovering new therapies targeting mitochondria for treating heart failure. Linked Articles This article is part of a themed section on Mitochondrial Pharmacology: Featured Mechanisms and Approaches for Therapy Translation. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.22/issuetoc

show abstract

Mitochondria and Cardiac Hypertrophy

Cited by 54 publications

References 161 publications

Application of Zebrafish Model in the Suppression of Drug-Induced Cardiac Hypertrophy by Traditional Indian Medicine Yogendra Ras

Application of Zebrafish Model in the Suppression of Drug-Induced Cardiac Hypertrophy by Traditional Indian Medicine Yogendra Ras

Pyrroloquinoline quinone attenuates isoproterenol hydrochloride‑induced cardiac hypertrophy in AC16 cells by inhibiting the NF‑κB signaling pathway

Three‐dimensional electron microscopy techniques for unravelling mitochondrial dysfunction in heart failure and identification of new pharmacological targets

Contact Info

Product

Resources

About