Mitochondrial-Shaping Proteins in Cardiac Health and Disease – the Long and the Short of It!

Ong, Sang‐Bing; Kalkhoran, Siavash Beikoghli; Hernández‐Reséndiz, Sauri; Samangouei, Parisa; Ong, Sang-Ging; Hausenloy, Derek J.

doi:10.1007/s10557-016-6710-1

Cited by 82 publications

(88 citation statements)

References 245 publications

(360 reference statements)

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“…According to the summary, we find that under I/R conditions, the actions of mitochondrial fusion proteins on cardiomyocyte apoptosis are tightly associated with the underlying mechanisms. Mitochondrial fusion proteins have fusion effects and non‐fusion effects (Burke, Hall, & Hausenloy, ; Ong et al, ). The protective effects of fusion proteins on cardiomyocytes upon I/R depend on their fusion effects.…”

Section: The Role Of Mitochondrial Fusion and Fission In Cardiomyocytmentioning

confidence: 99%

Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion

2018

Journal Cellular Physiology

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As the main source of energy in the body, mitochondria are highly dynamic organelles, which are constantly going through fusion and fission. The fine balance of mitochondrial fusion and fission plays an important role in maintaining the stability of cardiomyocyte homeostasis. The processes of mitochondrial fusion and fission are very complex, which is mediated by fusion and fission proteins. Disruptions in these processes through controlling fusion and fission proteins affect mitochondrial functions and cardiomyocyte survival. Ischemia/reperfusion (I/R) can regulate the expression and post‐translational modifications of fusion and fission proteins thereby inducing the abnormality of mitochondrial fusion and fission and cardiomyocyte apoptosis. Furthermore, intervention with the expression and function of fusion and fission proteins influences on cardiomyocyte apoptosis under I/R conditions. In this review, we focus on the current developments in the effects of mitochondrial fusion and fission on cardiomyocyte functions, the implications for cardiomyocyte apoptosis in response to I/R, and possible mechanisms. And we review their roles as a potential therapeutic target for treating I/R‐induced cardiomyocyte injury.

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Section: The Role Of Mitochondrial Fusion and Fission In Cardiomyocytmentioning

confidence: 99%

Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion

2018

Journal Cellular Physiology

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“…Several proteins are involved in fission and fusion and are referred to as “mitochondria‐shaping” proteins. These proteins include dynamin‐related protein 1 (Drp1) and the mitofusins, Mfn1 and Mfn2 . However, the importance of mitochondrial dynamics for cell fate has not been fully appreciated until recently.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial network structure homeostasis and cell death

et al. 2018

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Mitochondria are the major cellular energy‐producing organelles and intracellular source of reactive oxygen species. These organelles are responsible for driving cell life and death through mitochondrial network structure homeostasis, which is determined by a balance of fission and fusion. Recent advances revealed that a number of components of the fission and fusion machinery, including dynamin‐related protein 1 (Drp1), mitofusin1/2 (Mfn1/2) and Optic atrophy 1 (OPA1), that have been implicated in mitochondrial shape changes are indispensible for autophagy, apoptosis and necroptosis. Drp1 is the main regulator of mitochondrial fission and has become a key point of contention. The controversy focuses on whether Drp1 is directly involved in the regulation of cell death and, if involved, whether is it a stimulator or a negative regulator of cell death. Here, we examine the relevance of the homeostasis of the mitochondrial network structure in 3 different types of cell death, including autophagy, apoptosis and necroptosis. Furthermore, a variety of cancers often exhibit a fragmented mitochondrial phenotype. Thus, the fragmented ratio can reflect tumor progression that predicts prognosis and therapeutic response. In addition, we investigate whether the targeting of the mitochondrial fission protein Drp1 could be a novel therapeutic approach.

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“…The equilibrium of dynamic is largely dependent on MFF balance, which is crucial for mitochondrial homeostasis and cell health . Mitochondrial fission factor is known as a receptor to promote mitochondrial fission by recruitment Drp1 onto mitochondria membrane, and alteration of expression of MFF is related with cardiovascular diseases . Mitochondrial fission factor is directly inhibited by miR‐761 upon hydrogen peroxide treatment or ischemia/reperfusion injury .…”

Section: Discussionmentioning

confidence: 99%

miR‐376b‐3p attenuates mitochondrial fission and cardiac hypertrophy by targeting mitochondrial fission factor

Sun

Yang

et al. 2018

Clin Exp Pharma Physio

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Mitochondrial dysfunction contributes to the pathogenesis of cardiac hypertrophy. The disequilibrium of mitochondrial dynamic, which refers to mitochondrial fusion and fission, leads to mitochondrial morphology alteration and dysfunction. Enhanced understanding of the molecular mechanisms in depth may shed light on the therapy of the disease. In this study, we show that mitochondrial fission factor (MFF) is up-regulated upon hypertrophic agonist noradrenaline (NA) treatment. Knockdown of MFF attenuated NA induced mitochondrial fission and cardiac hypertrophy. Mitochondrial fission factor is a direct target of miR-376b-3p, which attenuated expression enhanced MFF expression through binding to its 3'UTR. Expression of miR-376b-3p weakened the fragmentation of mitochondria as well as decreased hypertrophic response through regulating MFF in NA treated neonatal rat ventricular cells (NRVCs). This study suggested that miR-376b-3p is a novel modulator affecting mitochondrial morphology through targeting MFF.

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Mitochondrial-Shaping Proteins in Cardiac Health and Disease – the Long and the Short of It!

Cited by 82 publications

References 245 publications

Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion

Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion

Mitochondrial network structure homeostasis and cell death

miR‐376b‐3p attenuates mitochondrial fission and cardiac hypertrophy by targeting mitochondrial fission factor

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