Cardiac metabolism in hypertrophy and heart failure: implications for therapy

Siddiqi, Nishat; Singh, Satnam; Beadle, Roger; Dawson, Dana; Frenneaux, Michael

doi:10.1007/s10741-012-9359-2

Cited by 20 publications

(17 citation statements)

References 98 publications

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“…Despite significant improvements in clinical diagnosis and efficiency of symptoms control, the progression of heart failure treatment remains unchanged with high rehospitalization rate. Novel therapeutic approaches are urgently needed [31]. Here, we provide an option of baicalin, which presents efficient attenuation of cardiac hypertrophy and mortality induced by pressure overload.…”

Section: Discussionmentioning

confidence: 99%

Baicalin Attenuates Cardiac Dysfunction and Myocardial Remodeling in a Chronic Pressure-Overload Mice Model

Zhang

Liao

Zhu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy remains unknown. Here we investigated the protective effects of baicalin on cardiac hypertrophy induced by pressure overload and explored the potential mechanisms involved. Methods: C57BL/6J-mice were treated with baicalin or vehicle following transverse aortic constriction or Sham surgery for up to 8 weeks, and at different time points, cardiac function and heart size measurement and histological and biochemical examination were performed. Results: Mice under pressure overload exhibited cardiac dysfunction, high mortality, myocardial hypertrophy, increased apoptosis and fibrosis markers, and suppressed cardiac expression of PPARα and PPARβ/δ. However, oral administration of baicalin improved cardiac dysfunction, decreased mortality, and attenuated histological and biochemical changes described above. These protective effects of baicalin were associated with reduced heart and cardiomyocyte size, lower fetal genes expression, attenuated cardiac fibrosis, lower expression of profibrotic markers, and decreased apoptosis signals in heart tissue. Moreover, we found that baicalin induced PPARα and PPARβ/δ expression in vivo and in vitro. Subsequent experiments demonstrated that long-term baicalin treatment presented no obvious cardiac lipotoxicity. Conclusions: The present results demonstrated that baicalin attenuates pressure overload induced cardiac dysfunction and ventricular remodeling, which would be due to suppressed cardiac hypertrophy, fibrosis, apoptosis and metabolic abnormality.

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Section: Discussionmentioning

confidence: 99%

Baicalin Attenuates Cardiac Dysfunction and Myocardial Remodeling in a Chronic Pressure-Overload Mice Model

Zhang

Liao

Zhu

et al. 2017

Cell Physiol Biochem

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“…improving mitochondrial electron transport chain (ETC) function; or increasing energy transfer from the mitochondrion to the cytosol (Siddiqi, et al, 2013). Agents have shown promise in HFrEF, include trimetazidine and perhexiline.…”

Section: Introductionmentioning

confidence: 99%

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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“…The cardiovascular system damages such as left ventricular hypertrophy and heart failure is quite common [16,17]. In addition, asymmetric septal hypertrophy which is a type of left ventricular hypertrophy is a common finding of hypertension.…”

Section: Discussionmentioning

confidence: 99%