FoxO1 is required for high glucose-dependent cardiac fibroblasts into myofibroblast phenoconversion

Vivar, Raúl; Anfossi, Renatto; Humeres, Claudio; Catalán, Mabel; Reyes, Christopher; Cárdenas, S Juan Pablo; Contreras, Alejandra; Aránguiz, Pablo; Gonzalez, F. Jesus; Díaz‐Araya, Guillermo

doi:10.1016/j.cellsig.2021.109978

Cited by 12 publications

(7 citation statements)

References 60 publications

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“…FoxO1 is a critical transcription factor in insulin cascade affected by different upstream signaling molecules [e.g., phosphatidylinositol 3-kinase (PI3K)/Akt, AMP-activated protein kinase (AMPK), and Sirtuin 1 (SIRT 1)], and it can regulate several downstream proteins, including myocardial pyruvate dehydrogenase (PDH) and peroxisome proliferator-activated receptor α (PPARγ) coactivator-1α (PGC-1α) (89)(90)(91)(92). In 2021, several studies proved inhibition of FoxO1 may be an approach to alleviate cardiac fibrosis, diastolic dysfunction, and left ventricular dysfunction and remodeling in the mouse model of DCM (93)(94)(95). Thus, FoxO1 could be an attractive target for the pharmacotherapy of DCM.…”

Section: Discussionmentioning

confidence: 99%

Research status and trends of the diabetic cardiomyopathy in the past 10 years (2012–2021): A bibliometric analysis

Wang

Tian²,

Gao³

et al. 2022

Front. Cardiovasc. Med.

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BackgroundDiabetic cardiomyopathy is one of the most life-threatening diabetic complications. However, the previous studies only discuss a particular aspect or characteristic of DCM, the current state and trends were explored by limited research. We aimed to perform a systemically bibliometric study of DCM research progress status in the past decade, visualize the internal conceptual structure and potential associations, and further explore the prospective study trends.MethodsArticles related to DCM published from January 2012 to December 2021 were collected in the Web of Science core collection (WoSCC) database on June 24, 2022. We exported all bibliographic records, including titles, abstracts, keywords, authorship, institutions, addresses, publishing sources, references, citation times, and year of publication. In addition, the journal Impact Factor and Hirsch index were obtained from the Journal Citation Report. We conducted the data screening, statistical analysis, and visualization via the Bibliometrix R package. VOS viewer software was employed to generate the collaboration network map among countries and institutions for better performance in visualization.ResultsIn total, 1,887 original research articles from 2012 to 2021 were identified. The number of annual publications rapidly increased from 107 to 278, and a drastic increase in citation times was observed in 2017–2019. As for global contributions, the United States was the most influential country with the highest international collaboration, while China was the most productive country. Professor Cai Lu was the most prolific author. Shandong University published the most articles. Cardiovascular Diabetology journal released the most DCM-related articles. “Metabolic Stress-induced Activation of FoxO1 Triggers Diabetic Cardiomyopathy in Mice” Battiprolu PK et al., J Clin Invest, 2012. was the most top-cited article regarding local citations. The top three keywords in terms of frequency were apoptosis, oxidative stress, and fibrosis. The analysis of future topic trends indicated that “Forkhead box protein O1,” “Heart failure with preserved ejection fraction,” “Dapagliflozin,” “Thioredoxin,” “Mitochondria dysfunction,” “Glucose,” “Pyroptosis,” “Cardiac fibroblast” and “Long non-coding RNA” could be promising hotspots.ConclusionThis study provides meaningful insights into DCM, which is expected to assist cardiologists and endocrinologists in exploring frontiers and future research directions in the domain through a refined and concise summary.

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Section: Discussionmentioning

confidence: 99%

Research status and trends of the diabetic cardiomyopathy in the past 10 years (2012–2021): A bibliometric analysis

Wang

Tian²,

Gao³

et al. 2022

Front. Cardiovasc. Med.

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“…U937 cells were washed with PBS and lysed as described previously ( 27 ). Total protein concentration was quantified with Bradford Assay.…”

Section: Methodsmentioning

confidence: 99%

Statins change the cytokine profile in Trypanosoma cruzi-infected U937 macrophages and murine cardiac tissue through Rho-associated kinases inhibition

et al. 2023

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IntroductionChronic Chagasic cardiomyopathy (CCC), caused by the protozoan Trypanosoma cruzi, is the most severe manifestation of Chagas disease.CCC is characterized by cardiac inflammation and fibrosis caused by a persistent inflammatory response. Following infection, macrophages secrete inflammatory mediators such as IL-1β, IL-6, and TNF-α to control parasitemia. Although this response contains parasite infection, it causes damage to the heart tissue. Thus, the use of immunomodulators is a rational alternative to CCC. Rho-associated kinase (ROCK) 1 and 2 are RhoA-activated serine/threonine kinases that regulate the actomyosin cytoskeleton. Both ROCKs have been implicated in the polarization of macrophages towards an M1 (pro-inflammatory) phenotype. Statins are FDA-approved lipid-lowering drugs that reduce RhoA signaling by inhibiting geranylgeranyl pyrophosphate (GGPP) synthesis. This work aims to identify the effect of statins on U937 macrophage polarization and cardiac tissue inflammation and its relationship with ROCK activity during T. cruzi infection.MethodsPMA-induced, wild-type, GFP-, CA-ROCK1- and CA-ROCK2-expressing U937 macrophages were incubated with atorvastatin, or the inhibitors Y-27632, JSH-23, TAK-242, or C3 exoenzyme incubated with or without T. cruzi trypomastigotes for 30 min to evaluate the activity of ROCK and the M1 and M2 cytokine expression and secretion profiling. Also, ROCK activity was determined in T. cruzi-infected, BALB/c mice hearts.ResultsIn this study, we demonstrate for the first time in macrophages that incubation with T. cruzi leads to ROCK activation via the TLR4 pathway, which triggers NF-κB activation. Inhibition of ROCKs by Y-27632 prevents NF-κB activation and the expression and secretion of M1 markers, as does treatment with atorvastatin. Furthermore, we show that the effect of atorvastatin on the NF-kB pathway and cytokine secretion is mediated by ROCK. Finally, statin treatment decreased ROCK activation and expression, and the pro-inflammatory cytokine production, promoting anti-inflammatory cytokine expression in chronic chagasic mice hearts.ConclusionThese results suggest that the statin modulation of the inflammatory response due to ROCK inhibition is a potential pharmacological strategy to prevent cardiac inflammation in CCC.

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“…6 Mechanism of myocardial fibroblasts on myocardial fibrosis in DCM Additionally, experiments in vitro also showed that HG can increase the expression and activity of TGF-b (162)(163)(164)(165). Stimulated by TGF-b, CFs play a key role in the fibrosis process of cardiac ECM remodeling by synthesizing and secreting various components of ECM, such as type I and type III collagen (8).…”

Section: Advanced Glycation End Products Affect Cardiac Fibroblastsmentioning

confidence: 99%

Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy

et al. 2023

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Diabetic cardiomyopathy (DCM), a main cardiovascular complication of diabetes, can eventually develop into heart failure and affect the prognosis of patients. Myocardial fibrosis is the main factor causing ventricular wall stiffness and heart failure in DCM. Early control of myocardial fibrosis in DCM is of great significance to prevent or postpone the progression of DCM to heart failure. A growing body of evidence suggests that cardiomyocytes, immunocytes, and endothelial cells involve fibrogenic actions, however, cardiac fibroblasts, the main participants in collagen production, are situated in the most central position in cardiac fibrosis. In this review, we systematically elaborate the source and physiological role of myocardial fibroblasts in the context of DCM, and we also discuss the potential action and mechanism of cardiac fibroblasts in promoting fibrosis, so as to provide guidance for formulating strategies for prevention and treatment of cardiac fibrosis in DCM.

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FoxO1 is required for high glucose-dependent cardiac fibroblasts into myofibroblast phenoconversion

Cited by 12 publications

References 60 publications

Research status and trends of the diabetic cardiomyopathy in the past 10 years (2012–2021): A bibliometric analysis

Research status and trends of the diabetic cardiomyopathy in the past 10 years (2012–2021): A bibliometric analysis

Statins change the cytokine profile in Trypanosoma cruzi-infected U937 macrophages and murine cardiac tissue through Rho-associated kinases inhibition

Central role of cardiac fibroblasts in myocardial fibrosis of diabetic cardiomyopathy

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