Compromised mitochondrial remodeling in compensatory hypertrophied myocardium of spontaneously hypertensive rat

Tang, Ying; Mi, Chunjuan; Liu, Jiankang; Gao, Feng; Long, Jiangang

doi:10.1016/j.carpath.2013.11.002

Cited by 58 publications

(42 citation statements)

References 36 publications

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“…In that study it was suggested that under basal conditions mitochondrial Sirtuin 3 deacetylates OPA1, thereby preserving the latter's function and maintaining mitochondrial fusion. Contrasting findings were, however, reported in a separate study which showed that total OPA1 expression was significantly increased in the compensatory LVH characteristic of the spontaneous hypertensive rat model (57).…”

Section: Opa1 and Left Ventricular Hypertrophycontrasting

confidence: 77%

OPA1 in Cardiovascular Health and Disease

Burke¹,

Hall²,

Hausenloy

2015

CDT

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Mitochondria are known to play crucial roles in normal cellular physiology and in more recent years they have been implicated in a wide range of pathologies. Central to both these roles is their ability to alter their shape interchangeably between two different morphologies: an elongated interconnected network and a fragmented discrete phenotype -processes which are under the regulation of the mitochondrial fusion and fission proteins, respectively. In this review article, we focus on the mitochondrial fusion protein optic atrophy protein 1 (OPA1) in cardiovascular health and disease and we explore its role as a potential therapeutic target for treating cardiovascular and metabolic disease.

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Section: Opa1 and Left Ventricular Hypertrophycontrasting

confidence: 77%

OPA1 in Cardiovascular Health and Disease

Burke¹,

Hall²,

Hausenloy

2015

CDT

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“…SIRT-1 is also down-regulated in HF (Fukushima & Lopaschuk, 2016). In spontaneously hypertensive rats, compensatory cardiac hypertrophy was accompanied by a decrease in SIRT-1 expression (Tang, et al, 2014). Similarly, SIRT-1 expression was reduced in patients with both compensated and decompensated HF (Akkafa, et al, 2015) and in patients with advanced HF (Lu, et al, 2014).…”

Section: Fatty Acid Metabolismmentioning

confidence: 77%

Cardiac metabolism — A promising therapeutic target for heart failure

Noordali

Loudon

Frenneaux

et al. 2018

Pharmacology & Therapeutics

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Both heart failure with reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF) are associated with high morbidity and mortality. Although many established pharmacological interventions exist for HFrEF, hospitalization and death rates remain high, and for those with HFpEF (approximately half of all heart failure patients), there are no effective therapies. Recently, the role of impaired cardiac energetic status in heart failure has gained increasing recognition with the identification of reduced capacity for both fatty acid and carbohydrate oxidation, impaired function of the electron transport chain, reduced capacity to transfer ATP to the cytosol, and inefficient utilization of the energy produced. These nodes in the genesis of cardiac energetic impairment provide potential therapeutic targets, and there is promising data from recent experimental and early-phase clinical studies evaluating modulators such as carnitine palmitoyltransferase 1 inhibitors, partial fatty acid oxidation inhibitors and mitochondrial-targeted antioxidants.Metabolic modulation may provide significant symptomatic and prognostic benefit for patients suffering from heart failure above and beyond guideline-directed therapy, but further clinical trials are needed.

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“…Mfn2 is reportedly increased after oxidant stress [9], but is decreased in diabetic hearts [10] and late after myocardial infarction [11]. And, Opa1 levels appeared to decrease in heart failure [12] and late after myocardial infarction [11], but were increased in hypertrophied hypertensive hearts [13] and in cardiomyocytes treated with insulin [14]. Mfn1, Mfn2, and Opa transcripts were all concordantly decreased in hearts having genetically-induced lipid overload [15].…”

Section: The Dynamism Of Cardiac Mitochondria Dynamics Proteinsmentioning

confidence: 99%

“…Consistent with its constitutive expression and induced mitochondrial localization/activation, cardiac Drp1 activity can be regulated postranslationally by activating (S616, S622) or inhibitory (S637) phosphorylation[17,18], activating SIRT3-dependent deacetylation (K926/931) [19], and activating O-GlcNAcylation [20] (Drp1 regulation is reviewed in detail in [21]). Cardiac Drp1 levels are decreased in chronically hypertrophied, hypertensive rat hearts [13], but cardiomyocyte Drp1 levels are increased by the pro-hypertrophic neurohormone norepinephrine [22]. Regulated cardiac expression of Drp1, Mfn1, Mfn2, and Opa1 have all been linked to transcriptional regulatory activity of PGC-1 [23].…”

Section: The Dynamism Of Cardiac Mitochondria Dynamics Proteinsmentioning

confidence: 99%

Mitochondrial fission/fusion and cardiomyopathy

Dorn

2016

Current Opinion in Genetics & Development

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Mitochondria are highly abundant in and essential to the beat-to-beat contractile performance of hearts. However, relatively few cardiac diseases have been attributed to primary mitochondrial dysfunction. The paucity of evidence for “primary mitochondrial cardiac diseases” may be because such an entity doesn’t exist. Alternately, the consequences of mitochondrial dysfunction on hearts may be so severe that long-term viability is severely impaired and affected individuals are therefore not included in standard genetic screens of adult heart disease subjects. Here, I review accumulating experimental evidence that impairing mitochondrial fission or fusion causes cardiomyopathy in otherwise normal mice, and consider how these data could motivate screening of perinatal cardiomyopathy subjects for damaging mutations of mitochondrial fission and fusion factors.

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Compromised mitochondrial remodeling in compensatory hypertrophied myocardium of spontaneously hypertensive rat

Cited by 58 publications

References 36 publications

OPA1 in Cardiovascular Health and Disease

OPA1 in Cardiovascular Health and Disease

Cardiac metabolism — A promising therapeutic target for heart failure

Mitochondrial fission/fusion and cardiomyopathy

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