Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: Therapeutic perspectives

Javadov, Sabzali; Jang, Sehwan; Agostini, Bryan

doi:10.1016/j.pharmthera.2014.05.013

Cited by 131 publications

(132 citation statements)

References 318 publications

(470 reference statements)

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“…In fact, many researchers have realized the association of mitogen-activated protein kinase (MAPK) involvement during DCM development. MAPK signaling pathways, such as extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK) and p38 MAP kinase, are demonstrated to be actively involved in myocardial dysfunction [9,10], hypertrophy [11,12,13], fibrosis [14,15,16] and heart failure [17,18,19]. As one MAPK family member, ERK1/2 has been known to be involved in cardiac hypertrophy [20,21].…”

Section: Introductionmentioning

confidence: 99%

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

Sun

Tong

et al. 2016

IJMS

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Diabetes mellitus is a chronic metabolic condition that affects carbohydrate, lipid and protein metabolism and may impair numerous organs and functions of the organism. Cardiac dysfunction afflicts many patients who experience the oxidative stress of the heart. Diabetic cardiomyopathy (DCM) is one of the major complications that accounts for more than half of diabetes-related morbidity and mortality cases. Chronic hyperglycemia and hyperlipidemia from diabetes mellitus cause cardiac oxidative stress, endothelial dysfunction, impaired cellular calcium handling, mitochondrial dysfunction, metabolic disturbances, and remodeling of the extracellular matrix, which ultimately lead to DCM. Although many studies have explored the mechanisms leading to DCM, the pathophysiology of DCM has not yet been fully clarified. In fact, as a potential mechanism, the associations between DCM development and mitogen-activated protein kinase (MAPK) activation have been the subjects of tremendous interest. Nonetheless, much remains to be investigated, such as tissue- and cell-specific processes of selection of MAPK activation between pro-apoptotic vs. pro-survival fate, as well as their relation with the pathogenesis of diabetes and associated complications. In general, it turns out that MAPK signaling pathways, such as extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK) and p38 MAP kinase, are demonstrated to be actively involved in myocardial dysfunction, hypertrophy, fibrosis and heart failure. As one of MAPK family members, the activation of ERK1/2 has also been known to be involved in cardiac hypertrophy and dysfunction. However, many recent studies have demonstrated that ERK1/2 signaling activation also plays a crucial role in FGF21 signaling and exerts a protective environment of glucose and lipid metabolism, therefore preventing abnormal healing and cardiac dysfunction. The duration, extent, and subcellular compartment of ERK1/2 activation are vital to differential biological effects of ERK1/2. Moreover, many intracellular events, including mitochondrial signaling and protein kinases, manipulate signaling upstream and downstream of MAPK, to influence myocardial survival or death. In this review, we will summarize the roles of ERK1/2 pathways in DCM development by the evidence from current studies and will present novel opinions on “differential influence of ERK1/2 action in cardiac dysfunction, and protection against myocardial ischemia-reperfusion injury”.

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Section: Introductionmentioning

confidence: 99%

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

Sun

Tong

et al. 2016

IJMS

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“…ERK5 is an atypical mitogen-activated protein kinase functioning as a transcriptional co-activator for PPARs and MEF2 in the heart. [95][96][97] SUMOylation of ERK5, which is strongly induced in diabetic animals, dampens its transcriptional activity. In diabetic mice, this was linked to ventricular dysfunction after myocardial infarction.…”

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confidence: 99%

The Ubiquitin-Like SUMO System and Heart Function

Mendler

Braun

Müller

2016

Circulation Research

101

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“…P-38 has an important function in cell-cell signaling against stress and is responsive to stress stimuli, such as cytokines, ultraviolet irradiation, heat shock, and osmotic shock. It is also involved in cell differentiation, apoptosis, and autophagy [36,37]. Similarly, NF-kB plays a very important role in several cellular functions.…”

Section: Resultsmentioning

confidence: 99%

Elucidation the Toxicity Mechanism of Zinc Oxide Nanoparticle Using Molecular Docking Approach With Proteins

Singh

Dhasmana

Rahman

2018

Asian J Pharm Clin Res

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Objective: At present, toxicological tests are resource-intensive, time-consuming and require a large pool of animal models for toxicity assessment. To speed up the toxicity evaluation and to reduce animal suffering during toxicity assessment, the use of alternative methods including computational models is in high demand. The computational toxicity prediction methods are very helpful for the regulatory bodies to quickly assess the health impact of nanomaterial materials. In the present work, we have examined the mechanism of zinc oxide nanoparticle (ZnO-NP)-proteins interaction and their effect of surface chemistries of ZnO-NP on the bioactive conformation of chemokines and other cytological proteins using in silico molecular docking approaches.Methods: Molecular docking study was conducted using AutoDock 4.0 version and the visualization result using Discover Studio 4.0. Results:In the present study, we observed that ZnO-NP has high binding affinity with the mitogen-activated protein kinases (P-38), nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) proteins, and matrix metallopeptidase-9 with docking energies −8.81, −7.64, and −7.27 Kcal/Mol, respectively, involving with hydrogen, metal acceptor, and electrostatic interaction. The top interacting amino acid residues with ZnO-NP are GLY, PHE, ARG, ASP, GLN, and ASN. Conclusion:Thus, based on the molecular docking studies, we determine that the ZnO-NP is strongly interacting with the chemokines and other cytological proteins thus responsible for blocking of the activation stimuli for these proteins to initiate the biological signals for the proper functioning. We have also extracted the information of interaction pattern of ZnO-NP with the surface-enriched amino acid residues of chemokine and cytological proteins using molecular docking approach.

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Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: Therapeutic perspectives

Cited by 131 publications

References 318 publications

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

The Ubiquitin-Like SUMO System and Heart Function

Elucidation the Toxicity Mechanism of Zinc Oxide Nanoparticle Using Molecular Docking Approach With Proteins

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