Lipotoxicity: a driver of heart failure with preserved ejection fraction?

Leggat, Jennifer; Bidault, Guillaume; Vidal-Puig, António

doi:10.1042/cs20210127

Cited by 27 publications

(16 citation statements)

References 158 publications

(170 reference statements)

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“… 42 Lipotoxicity is a process by which lipid accumulation in non-adipose organs results in oxidative stress, mitochondrial dysfunction, and apoptosis, leading to cellular and tissue dysfunction. 43 , 44 Sustained CD36 elevation may be responsible for the continued cardiac dysfunction through the induction of self-perpetuating changes in gene expression. miR-320 knockdown inhibited this regulatory loop and effectively rescued the diastolic dysfunction in type 1 and type 2 diabetic mice.…”

Section: Discussionmentioning

confidence: 99%

Positive feedback loop of miR-320 and CD36 regulates the hyperglycemic memory-induced diabetic diastolic cardiac dysfunction

Zhan¹,

Jin²,

Ding³

et al. 2023

Molecular Therapy - Nucleic Acids

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Section: Discussionmentioning

confidence: 99%

Positive feedback loop of miR-320 and CD36 regulates the hyperglycemic memory-induced diabetic diastolic cardiac dysfunction

Zhan¹,

Jin²,

Ding³

et al. 2023

Molecular Therapy - Nucleic Acids

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“…FAs can passively transfer across the cardiomyocytic plasma membrane to be utilized for cardiac ATP production, but their absorption is aided by both the FA translocase (CD36) and the FA binding protein (FABP) [ 52 ]. Carnitine palmitoyltransferase I (CPT1) converts FAs in the cytosol to long-chain acylcarnitine before they enter the mitochondria, where they are reversed to acyl-CoA by CPT2 and undergo β-oxidation [ 52 ]. Cytosolic FAs, on the other hand, can be esterified to produce triglycerides for storage in the myocardial triglyceride (TG) pool [ 52 ].…”

Section: Major Mechanisms In Heart Failure Pathophysiologymentioning

confidence: 99%

Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

Theofilis

Oikonomou

Tsioufis

et al. 2023

Life

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Diabetes mellitus (DM) and heart failure (HF) are frequently encountered afflictions that are linked by a common pathophysiologic background. According to landmark studies, those conditions frequently coexist, and this interaction represents a poor prognostic indicator. Based on mechanistic studies, HF can be propagated by multiple pathophysiologic pathways, such as inflammation, oxidative stress, endothelial dysfunction, fibrosis, cardiac autonomic neuropathy, and alterations in substrate utilization. In this regard, DM may augment myocardial inflammation, fibrosis, autonomic dysfunction, and lipotoxicity. As the interaction between DM and HF appears critical, the new cornerstone in DM and HF treatment, sodium-glucose cotransporter-2 inhibitors (SGLT2i), may be able to revert the pathophysiology of those conditions and lead to beneficial HF outcomes. In this review, we aim to highlight the deleterious pathophysiologic interaction between DM and HF, as well as demonstrate the beneficial role of SGLT2i in this field.

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“…In lipodystrophy syndromes, the very limited adipose tissue expandability, due to the major decrease in the capacity of adipose tissue to store lipids, exposes non-adipose organs to lipotoxicity even in well-balanced diet conditions. This results in muscle insulin resistance due to disruption of insulin signaling (24), in non-alcoholic fatty liver disease, as well as in myocardial, endothelial and pancreatic beta-cell dysfunction (25)(26)(27). Adipocytes are also important autocrine, paracrine, and endocrine cells that produce numerous adipokines.…”

Section: Lipodystrophy and Lipotoxicitymentioning

confidence: 99%

Molecular and Cellular Bases of Lipodystrophy Syndromes

et al. 2022

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Lipodystrophy syndromes are rare diseases originating from a generalized or partial loss of adipose tissue. Adipose tissue dysfunction results from heterogeneous genetic or acquired causes, but leads to similar metabolic complications with insulin resistance, diabetes, hypertriglyceridemia, nonalcoholic fatty liver disease, dysfunctions of the gonadotropic axis and endocrine defects of adipose tissue with leptin and adiponectin deficiency. Diagnosis, based on clinical and metabolic investigations, and on genetic analyses, is of major importance to adapt medical care and genetic counseling. Molecular and cellular bases of these syndromes involve, among others, altered adipocyte differentiation, structure and/or regulation of the adipocyte lipid droplet, and/or premature cellular senescence. Lipodystrophy syndromes frequently present as systemic diseases with multi-tissue involvement. After an update on the main molecular bases and clinical forms of lipodystrophy, we will focus on topics that have recently emerged in the field. We will discuss the links between lipodystrophy and premature ageing and/or immuno-inflammatory aggressions of adipose tissue, as well as the relationships between lipomatosis and lipodystrophy. Finally, the indications of substitutive therapy with metreleptin, an analog of leptin, which is approved in Europe and USA, will be discussed.

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Lipotoxicity: a driver of heart failure with preserved ejection fraction?

Cited by 27 publications

References 158 publications

Positive feedback loop of miR-320 and CD36 regulates the hyperglycemic memory-induced diabetic diastolic cardiac dysfunction

Positive feedback loop of miR-320 and CD36 regulates the hyperglycemic memory-induced diabetic diastolic cardiac dysfunction

Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

Molecular and Cellular Bases of Lipodystrophy Syndromes

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