Crosstalk between Autophagy and Apoptosis: Potential and Emerging Therapeutic Targets for Cardiac Diseases

Li, Meng; Gao, Ping; Zhang, Junping

doi:10.3390/ijms17030332

Cited by 133 publications

(124 citation statements)

References 142 publications

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“…The mitochondrial pathway can be activated by several stimuli including growth factors, oxidative stress, DNA damage and hypoxia (101). Following activation of apoptosis, proteins in the Bcl-2 protein family regulate mitochondria membrane integrity and permeability.…”

Section: Apoptosismentioning

confidence: 99%

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Steiner

Lang

2017

The International Journal of Biochemistry & Cell Biology

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Putative mechanisms leading to the development of alcoholic cardiomyopathy (ACM) include the interrelated cellular processes of mitochondria metabolism, oxidative stress and apoptosis. As mitochondria fuel the constant energy demands of this continually contracting tissue, it is not surprising that alcohol-induced molecular changes in this organelle contribute to cardiac dysfunction and ACM. As the causal relationship of these processes with ACM has already been established, the primary objective of this review is to provide an update of the experimental findings to more completely understand the aforementioned mechanisms. Accordingly, recent data indicate that alcohol impairs mitochondria function assessed by membrane potential and respiratory chain activity. Indictors of oxidative stress including superoxide dismutase, glutathione metabolites and malondialdehyde are also adversely affected by alcohol oftentimes in a sex-dependent manner. Additionally, myocardial apoptosis is increased based on assessment of TUNEL staining and caspase activity. Recent work has also emerged linking alcohol-induced oxidative stress with apoptosis providing new insight on the codependence of these interrelated mechanisms in ACM. Attention is also given to methodological differences including the dose of alcohol, experimental model system and the use of males versus females to highlight inconsistencies and areas that would benefit from establishment of a consistent model.

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Section: Apoptosismentioning

confidence: 99%

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Steiner

Lang

2017

The International Journal of Biochemistry & Cell Biology

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“…It has been demonstrated that an intense cross-talking between autophagy, apoptosis, and necrosis in the protozoa in response to diverse drug stimuli that cover the same pathway of the previous processes [2]. Intriguingly, in the light of the fact that apoptosis and autophagy are interconnected, a significant analysis and discussion on the proteins with a dual role in autophagy and apoptosis were presented by Li et al and Tait et al [3,4]. Furthermore, several recent studies have reported the continuity of apoptosis and necrosis stemming from the diversion of the core apoptotic pathway by intracellular ATP and caspase depletion [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Cell death offers exceptional cellular and molecular windows for pharmacological interventions in protozoan parasites

El‐Ashram¹,

Mehmood²,

Dinçel³

et al. 2017

Integr Mol Med

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The rich repertoire of cell death events is a crucial biological process that deserves extensive review at a formative time for the development of our knowledge concerning the state-of-the-art data on their cellular and molecular mechanisms of action and the ways in which they can be manipulated in and by protozoan parasites. We have attempted to provide a comprehensive overview to reveal intervention points that could be exploited to discover novel therapies, vaccine strategies and prophylactic intervention points for protozoan parasites, and to understand the parasitic disease progression and the infection consequence.

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“…The fundamental function of autophagy is to maintain the metabolic balance in the cell, since autophagy is able to produce essential nutrients such as amino acids under various stress conditions, including nutrient starvation, oxidative stress and endoplasmic reticulum stress (7). Autophagy is beneficial for repair after injury; however, it is also known to also have unfavorable results.…”

Section: Introductionmentioning

confidence: 99%

Overactivated autophagy contributes to steroid-induced avascular necrosis of the femoral head

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Steroid-induced avascular necrosis of the femoral head (SANFH) is a mainly bilateral complication of steroid therapy that involves extensive necrosis, and frequently occurs in young and middle-aged individuals, with a high disability rate. Autophagy is an intracellular lysosomal degradation process occurring in numerous diseases. However, the effect of dexamethasone (DXM)-induced autophagy on osteoblasts is unclear. The aim of the present study was to investigate the effects of autophagy on SANFH. In the present study, femoral head of SANFH patients was collected, and the autophagy in the samples was evaluated. In addition, cell proliferation, membrane integrity and differentiation of osteoblasts were also detected to confirm the effect of DXM on a mouse osteoblasts cell MC3T3-E1 in vitro. Beclin 1 and microtubule-associated protein 1 light chain 3 were used as the markers of autophagy, while the autophagy inhibitor 3-methyladenine (3-MA) was used to investigate the role of autophagy in DXM-challenged osteoblasts. Immunohistochemistry results demonstrated that Beclin1 was markedly increased in the femoral head of SANFH patients. Furthermore, the treatment of osteoblasts with DXM decreased cell viability, increased lactate dehydrogenase activity in the cell culture supernatant, and reduced the alkaline phosphatase activity and bone morphogenetic protein-2 expression in osteoblasts in vitro. By contrast, 3-MA treatment attenuated the cell injury induced by DXM. The present study indicates that overactivated autophagy may be an important factor contributing to SANFH, and autophagy may be a potential target for the prevention of SANFH.

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Crosstalk between Autophagy and Apoptosis: Potential and Emerging Therapeutic Targets for Cardiac Diseases

Cited by 133 publications

References 142 publications

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Cell death offers exceptional cellular and molecular windows for pharmacological interventions in protozoan parasites

Overactivated autophagy contributes to steroid-induced avascular necrosis of the femoral head

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