Mitochondrial remodeling: Rearranging, recycling, and reprogramming

Gottlieb, Roberta A.; Bernstein, Daniel

doi:10.1016/j.ceca.2016.04.006

Cited by 77 publications

(60 citation statements)

References 218 publications

(228 reference statements)

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“…These mechanisms may include mitochondrial fission or fusion, in which damaged parts of mitochondria are excised and smaller mitochondria fuse to create larger mitochondria. 56,57 Drp1 is a pivotal protein in mediating mitochondrial fission as it has the capacity to constrict mitochondria. In the context of HCV infection, it has been demonstrated that mitochondrial localization of phosphorylated form of Drp1 protein (Drp1-Ser616) was a prelude to mitochondrial fission.…”

Section: Discussionmentioning

confidence: 99%

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

et al. 2017

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Mitochondria are sentinel organelles that are impacted by various forms of cellular stress, including viral infections. While signaling events associated with mitochondria, including those activated by pathogen associated molecular patterns (PAMPs), are widely studied, alterations in mitochondrial distribution and changes in mitochondrial dynamics are also beginning to be associated with cellular insult. Cells of neuronal origin have been demonstrated to display remarkable alterations in several instances, including neurodegenerative disorders. Venezuelan Equine Encephalitis Virus (VEEV) is a New World alphavirus that infects neuronal cells and contributes to an encephalitic phenotype. We demonstrate that upon infection by the vaccine strain of VEEV (TC-83), astrocytoma cells experience a robust drop in mitochondrial activity, which corresponds with an increased accumulation of reactive oxygen species (ROS) in an infection-dependent manner. Infection status also corresponds with a prominent perinuclear accumulation of mitochondria. Cellular enzymatic machinery, including PINK1 and Parkin, appears to be enriched in mitochondrial fractions as compared with uninfected cells, which is indicative of mitochondrial damage. Dynamin related protein 1 (Drp1), a protein that is associated with mitochondrial fission, demonstrated a modest enrichment in mitochondrial fractions of infected cells. Treatment with an inhibitor of mitochondrial fission, Mdivi-1, led to a decrease in caspase cleavage, suggesting that mitochondrial fission was likely to contribute to apoptosis of infected cells. Finally, our data demonstrate that mitophagy ensues in infected cells. In combination, our data suggest that VEEV infection results in significant changes in the mitochondrial landscape that may influence pathological outcomes in the infected cell.

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Section: Discussionmentioning

confidence: 99%

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

et al. 2017

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“…A role for mitochondria and ER is suggested in the latter process. Gottlieb and Bernstein [33] contribute an interesting review that discusses mitochondrial remodeling and mechanisms that govern its rearranging, recycling, and reprogramming. Mitochondria adapt to a wide range of cellular requirements, adjusting fuel utilization to meet ATP requirements and regulating ROS output.…”

Section: Ros and Intracellular Ca2+ Signalingmentioning

confidence: 99%

ROS and Ca 2+ —Partners in sickness and in health

Ambudkar

Muallem

2016

Cell Calcium

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“…p62, which orchestrate organellar engulfment by the autophagosome. 31 The pro-apoptotic BH3-only proteins Bnip3 and Nix have recently been demonstrated to also function as adaptors for recruiting mitochondria to the autophagosome, by interacting with LC3. 32 In non-cardiac cell types, the adaptor proteins NDP52 and Optineurin have been found to participate in mitophagy, 33 undergoing recruitment to mitochondria in a Pink1-dependent but Parkin-independent manner.…”

Section: Cargo-selective Autophagy: Macro-autophagy Subtypesmentioning

confidence: 99%

Myocardial stress and autophagy: mechanisms and potential therapies

et al. 2017

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Autophagy is a ubiquitous cellular catabolic process responsive to energy stress status. Research over the last decade has revealed that cardiomyocyte autophagy is a prominent homeostatic pathway, important in adaptation to altered myocardial metabolic demand. The cellular machinery of autophagy involves targeted direction of macromolecules and organelles for lysosomal degradation. Autophagy activation has been identified as cardio-protective in some settings (i.e. ischemia and ischemic preconditioning). In other situations chronically elevated levels of autophagy have been linked with cardiopathology (i.e. sustained pressure overload and failure). Autophagy perturbation in diabetic cardiomyopathy is also observed – and has been associated with both adaptive and maladaptive stress responses. Recent findings indicate that various forms of selective autophagy operate in parallel to manage different catabolic ‘cargo’ types including mitochondria, large proteins, glycogen and lipid stores. In this Review, specific circumstances of autophagy induction associated with cardiac benefit or detriment are considered. The various static and dynamic approaches used for measurement of autophagy are critiqued and current inconsistencies in the understanding of autophagy regulation in the heart are highlighted. The future prospects for pharmacological intervention to achieve therapeutic manipulation of autophagic processes are canvassed.

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Mitochondrial remodeling: Rearranging, recycling, and reprogramming

Cited by 77 publications

References 218 publications

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

ROS and Ca 2+ —Partners in sickness and in health

Myocardial stress and autophagy: mechanisms and potential therapies

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