Author Correction: Macrophage-dependent IL-1β production induces cardiac arrhythmias in diabetic mice

Monnerat, Gustavo; Alarcón, Micaela López; Vasconcellos, Luiz Ricardo; Hochman-Mendez, Camila; Brasil, Guilherme Visconde; Bassani, Rosana A.; Casis, Óscar; Malan, Daniela; Travassos, Leonardo H.; Sepúlveda, Marisa Noemí; Burgos, Juan Ignacio; Petroff, Martín Gerardo Vila; Dutra, Fabiano F.; Bozza, Marcelo T.; Paiva, Cláudia N.; Carvalho, Adriana Bastos; Bonomo, Adriana; Fleischmann, Bernd K.; Carvalho, Antônio Carlos Campos de; Medei, Emiliano

doi:10.1038/s41467-021-27508-w

Cited by 5 publications

(4 citation statements)

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“…In addition to CRS, the potent inflammatory IL-1β promotes fibroblast migration, 137 affects the action potential of cardiomyocytes, and changes their electrical functions. 138 In contrast, IL-6 increases fibroblast proliferation and cardiac fibrosis. 139 These inflammatory cytokines are also necessary to clean-up several processes in the ischemic heart and reverse the tendency to postinfarct heart conduction disorders.…”

Section: Car Constructsmentioning

confidence: 99%

“…It should be mentioned that chronic HF patients are frequently associated with an advanced inflammatory state, and excess inflammation may complicate the condition of cardiac damage. In addition to CRS, the potent inflammatory IL‐1β promotes fibroblast migration, 137 affects the action potential of cardiomyocytes, and changes their electrical functions 138 . In contrast, IL‐6 increases fibroblast proliferation and cardiac fibrosis 139 .…”

Section: Roadblocks Of Car T Cell Therapy In Cardiac Fibrosismentioning

confidence: 99%

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CAR‐T cell therapeutic avenue for fighting cardiac fibrosis: Roadblocks and perspectives

Abdalla,

Miao,

Ahmed

et al. 2024

Cell Biochemistry & Function

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Heart diseases remain the primary cause of human mortality in the world. Although conventional therapeutic opportunities fail to halt or recover cardiac fibrosis, the promising clinical results and therapeutic efficacy of engineered chimeric antigen receptor (CAR) T cell therapy show several advancements. However, the current models of CAR‐T cells need further improvement since the T cells are associated with the triggering of excessive inflammatory cytokines that directly affect cardiac functions. Thus, the current study highlights the critical function of heart immune cells in tissue fibrosis and repair. The study also confirms CAR‐T cell as an emerging therapeutic for treating cardiac fibrosis, explores the current roadblocks to CAR‐T cell therapy, and considers future outlooks for research development.

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Section: Car Constructsmentioning

confidence: 99%

Section: Roadblocks Of Car T Cell Therapy In Cardiac Fibrosismentioning

confidence: 99%

CAR‐T cell therapeutic avenue for fighting cardiac fibrosis: Roadblocks and perspectives

Abdalla,

Miao,

Ahmed

et al. 2024

Cell Biochemistry & Function

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“…In the diabetic mouse model, the elevated levels of NLRP3 activate macrophages to secrete IL-1β. This secretion induces a decrease in potassium current and an increase in calcium current in cardiomyocytes by prolonging the action potential duration, ultimately promoting cardiac fibrosis [ 191 ]. In addition to simply promoting fibrosis, macrophages can exhibit different fibrotic effects at different stages; in the inflammatory model of the heart, the increased secretion of MMP9 by macrophages enhances the expression of Mer tyrosine kinase in the early stage of inflammation.…”

Section: Crosstalk Between Myocytes and Non-myocyte Cells In Cardiac ...mentioning

confidence: 99%

Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis

Chu,

Xie,

2023

Biomolecules

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Epigenetic mechanisms and cell crosstalk have been shown to play important roles in the initiation and progression of cardiac fibrosis. This review article aims to provide a thorough overview of the epigenetic mechanisms involved in fibroblast regulation. During fibrosis, fibroblast epigenetic regulation encompasses a multitude of mechanisms, including DNA methylation, histone acetylation and methylation, and chromatin remodeling. These mechanisms regulate the phenotype of fibroblasts and the extracellular matrix composition by modulating gene expression, thereby orchestrating the progression of cardiac fibrosis. Moreover, cardiac fibrosis disrupts normal cardiac function by imposing myocardial mechanical stress and compromising cardiac electrical conduction. This review article also delves into the intricate crosstalk between cardiomyocytes and non-cardiomyocytes in the heart. A comprehensive understanding of the mechanisms governing epigenetic regulation and cell crosstalk in cardiac fibrosis is critical for the development of effective therapeutic strategies. Further research is warranted to unravel the precise molecular mechanisms underpinning these processes and to identify potential therapeutic targets.

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“…A chronic inflammatory response clearly persists in diabetes through deadly activating the innate immune system to damage the heart ( 20 , 111 ). Some early-responding pro-inflammatory immune cells, like M1-polarized macrophages, lymphocytes and neutrophils, secrete IL-6, IL-18, TNF-α, IL-1β to attack vascular smooth muscle cells, fibroblasts and cardiomyocytes impairing cellular energy metabolism and cause cardiovascular dysfunction ( 112 , 113 ). TLR4 can be activated by the excess free fatty acid and pathogen-associated molecular patterns (PAMPs) to induce the synthesis of pro-inflammatory cytokines, meanwhile the activation of NF-κB by TLR4 also amplify the inflammatory response and pathological alterations ( Figure 4 ) ( 114 ).…”

Section: Inflammatory Response and Oxidative Stress In Dcmmentioning

confidence: 99%

Profile of crosstalk between glucose and lipid metabolic disturbance and diabetic cardiomyopathy: Inflammation and oxidative stress

et al. 2022

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In recent years, the risk, such as hypertension, obesity and diabetes mellitus, of cardiovascular diseases has been increasing explosively with the development of living conditions and the expansion of social psychological pressure. The disturbance of glucose and lipid metabolism contributes to both collapse of myocardial structure and cardiac dysfunction, which ultimately leads to diabetic cardiomyopathy. The pathogenesis of diabetic cardiomyopathy is multifactorial, including inflammatory cascade activation, oxidative/nitrative stress, and the following impaired Ca2+ handling induced by insulin resistance/hyperinsulinemia, hyperglycemia, hyperlipidemia in diabetes. Some key alterations of cellular signaling network, such as translocation of CD36 to sarcolemma, activation of NLRP3 inflammasome, up-regulation of AGE/RAGE system, and disequilibrium of micro-RNA, mediate diabetic oxidative stress/inflammation related myocardial remodeling and ventricular dysfunction in the context of glucose and lipid metabolic disturbance. Here, we summarized the detailed oxidative stress/inflammation network by which the abnormality of glucose and lipid metabolism facilitates diabetic cardiomyopathy.

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Author Correction: Macrophage-dependent IL-1β production induces cardiac arrhythmias in diabetic mice

Cited by 5 publications

References 0 publications

CAR‐T cell therapeutic avenue for fighting cardiac fibrosis: Roadblocks and perspectives

CAR‐T cell therapeutic avenue for fighting cardiac fibrosis: Roadblocks and perspectives

Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis

Profile of crosstalk between glucose and lipid metabolic disturbance and diabetic cardiomyopathy: Inflammation and oxidative stress

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