FABP5 Deficiency Impairs Mitochondrial Function and Aggravates Pathological Cardiac Remodeling and Dysfunction

Gao, Shanquan; Li, Guoqi; Shao, Yihui; Wei, Zhipeng; Huang, Shan; Qi, Feiran; Yao, Jiao; Li, Yulin; Zhang, Congcong; Du, Jie

doi:10.1007/s12012-021-09653-2

Cited by 19 publications

(16 citation statements)

References 39 publications

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“…On the other hand, our study found that FABP5 inhibition could improve cardiac function in this MI-induced heart failure model, which is inconsistent with findings from a pressure-overload heart failure model [39] . Gao et al recently reported decreased cardiac function in FABP5 knockout mice with transverse aortic constriction (TAC)-induced heart failure [39] . Discrepancy between the studies may derive from distinct types of mouse model.…”

Section: Discussioncontrasting

confidence: 99%

“…In contrast, Gao et al investigated the role of FABP5 in TAC-induced heart failure in the FABP5 knockout mice, where myocardial hypertrophy and mitochondrial dysfunction are the main pathology. In this setting, the myocardial deficiency of FABP5 could accelerate the mitochondrial dysfunction and therefore aggravate heart dysfunction [39] . Since FABP5 can regulate inflammation process, which is critical for heart failure progression after MI, FABP5 may also affect cardiac function through modulating inflammatory response in the setting of MI.…”

Section: Discussionmentioning

confidence: 99%

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Fatty acid-binding protein 5 aggravates pulmonary artery fibrosis in pulmonary hypertension secondary to left heart disease via activating wnt/β-catenin pathway

Lei

et al. 2022

Journal of Advanced Research

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Fatty acid-binding protein 5 aggravates pulmonary artery fibrosis in pulmonary hypertension secondary to left heart disease via activating wnt/β-catenin pathway

Lei

et al. 2022

Journal of Advanced Research

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“…Fabp5 coding for the Fatty acid binding protein 5, involved in lipid transport and a potential protective mechanism against pathological remodeling [ 84 ], was markedly elevated in ECH and HF macrophages, as compared to Ct counterparts ( Figure 5 ). A similar regulation was detected for genes such as Mmp14 (matrix metalloproteinase 14), a candidate lipophagy regulator [ 81 ] and Mif (macrophage migration inhibitory factor), a cardioprotective activator of autophagy reported to mitigate pathological hypertrophic responses [ 85 ] ( Figure 5 ).…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic and Lipidomic Mapping of Macrophages in the Hub of Chronic Beta-Adrenergic-Stimulation Unravels Hypertrophy-, Proliferation-, and Lipid Metabolism-Related Genes as Novel Potential Markers of Early Hypertrophy or Heart Failure

et al. 2022

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Sympathetic nervous system overdrive with chronic release of catecholamines is the most important neurohormonal mechanism activated to maintain cardiac output in response to heart stress. Beta-adrenergic signaling behaves first as a compensatory pathway improving cardiac contractility and maladaptive remodeling but becomes dysfunctional leading to pathological hypertrophy and heart failure (HF). Cardiac remodeling is a complex inflammatory syndrome where macrophages play a determinant role. This study aimed at characterizing the temporal transcriptomic evolution of cardiac macrophages in mice subjected to beta-adrenergic-stimulation using RNA sequencing. Owing to a comprehensive bibliographic analysis and complementary lipidomic experiments, this study deciphers typical gene profiles in early compensated hypertrophy (ECH) versus late dilated remodeling related to HF. We uncover cardiac hypertrophy- and proliferation-related transcription programs typical of ECH or HF macrophages and identify lipid metabolism-associated and Na+ or K+ channel-related genes as markers of ECH and HF macrophages, respectively. In addition, our results substantiate the key time-dependent role of inflammatory, metabolic, and functional gene regulation in macrophages during beta-adrenergic dependent remodeling. This study provides important and novel knowledge to better understand the prevalent key role of resident macrophages in response to chronically activated beta-adrenergic signaling, an effective diagnostic and therapeutic target in failing hearts.

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“…In healthy cardiomyocytes, mitochondria are abundant and contain intact membranes and clear cristae structures. In hypertrophic hearts subject to chronic overload, mitochondrial density is decreased, and the organelles may become swollen, elongated, and deformed, exhibiting ruptured membranes and irregular cristae structures [ 252 , 253 ] . These deformities reduce the biogenetic capacity of the mitochondria in the hypertrophic heart, which further exacerbates the detrimental effects of cardiac structural remodeling and may contribute significantly to the progression into the decompensated stage of PO-induced heart failure.…”

Section: Cardiac Remodeling Alters Mitochondrial Bioenergeticsmentioning

confidence: 99%

The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure

et al. 2023

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This review provides a holistic perspective on the bi-directional relationship between cardiac mitochondrial dysfunction and myocardial structural remodeling in the context of metabolic heart disease, natural cardiac aging, and heart failure. First, a review of the physiologic and molecular drivers of cardiac mitochondrial dysfunction across a range of increasingly prevalent conditions such as metabolic syndrome and cardiac aging is presented, followed by a general review of the mechanisms of mitochondrial quality control (QC) in the heart. Several important mechanisms by which cardiac mitochondrial dysfunction triggers or contributes to structural remodeling of the heart are discussed: accumulated metabolic byproducts, oxidative damage, impaired mitochondrial QC, and mitochondrial-mediated cell death identified as substantial mechanistic contributors to cardiac structural remodeling such as hypertrophy and myocardial fibrosis. Subsequently, the less studied but nevertheless important reverse relationship is explored: the mechanisms by which cardiac structural remodeling feeds back to further alter mitochondrial bioenergetic function. We then provide a condensed pathogenesis of several increasingly important clinical conditions in which these relationships are central: diabetic cardiomyopathy, age-associated declines in cardiac function, and the progression to heart failure, with or without preserved ejection fraction. Finally, we identify promising therapeutic opportunities targeting mitochondrial function in these conditions.

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FABP5 Deficiency Impairs Mitochondrial Function and Aggravates Pathological Cardiac Remodeling and Dysfunction

Cited by 19 publications

References 39 publications

Fatty acid-binding protein 5 aggravates pulmonary artery fibrosis in pulmonary hypertension secondary to left heart disease via activating wnt/β-catenin pathway

Fatty acid-binding protein 5 aggravates pulmonary artery fibrosis in pulmonary hypertension secondary to left heart disease via activating wnt/β-catenin pathway

Transcriptomic and Lipidomic Mapping of Macrophages in the Hub of Chronic Beta-Adrenergic-Stimulation Unravels Hypertrophy-, Proliferation-, and Lipid Metabolism-Related Genes as Novel Potential Markers of Early Hypertrophy or Heart Failure

The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure

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