The Microenvironment of Decellularized Extracellular Matrix from Heart Failure Myocardium Alters the Balance between Angiogenic and Fibrotic Signals from Stromal Primitive Cells

Belviso, Immacolata; Angelini, Francesco; Meglio, Franca Di; Picchio, Vittorio; Sacco, Anna Maria; Nocella, Cristina; Romano, Veronica; Nurzynska, Daria; Frati, Giacomo; Maiello, Ciro; Messina, Elisa; Montagnani, Stefania; Pagano, Francesca; Castaldo, Clotilde; Chimenti, Isotta

doi:10.3390/ijms21217903

Cited by 26 publications

(22 citation statements)

References 63 publications

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“…In fact, previous studies showed that CSCs can exert beneficial effects in the injured myocardium, mostly by positive microenvironmental conditioning through paracrine factors, which are able to render activated fibroblasts anti-fibrotic, and to polarize macrophages towards M2-like anti-inflammatory features [ 24 , 26 , 55 – 58 ]. Moreover, CSC phenotype can shift from cardioprotective features towards a pro-inflammatory and pro-fibrotic behaviour in response to different cues [ 29 , 33 , 59 , 60 ]. This phenotypic shift within the heterogeneous stromal population may significantly affect adaptation and therapeutic mechanisms in response to stress and injury [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…These benefits on tissue repair, however, depend on specific features of CSCs. In fact, myocardial remodelling and cardiovascular risk factors, such as diabetes [ 28 ], may lead to pro-fibrotic polarization and loss of the reparative potential of CSCs [ 29 , 30 ], with impaired paracrine potency [ 31 – 33 ]. Overall, the health status, comorbidities, and ongoing therapies of a patient can strongly affect the phenotype of CSCs [ 30 – 32 , 34 ], and in this way their direct and indirect contribution to fibrosis and remodelling.…”

Section: Introductionmentioning

confidence: 99%

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The impact of autophagy modulation on phenotype and survival of cardiac stromal cells under metabolic stress

Chimenti

Picchio

Pagano³

et al. 2022

Cell Death Discov.

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Cardiac stromal cells (CSCs) embrace multiple phenotypes and are a contributory factor in tissue homeostasis and repair. They can be exploited as therapeutic mediators against cardiac fibrosis and remodeling, but their survival and cardioprotective properties can be decreased by microenvironmental cues. We evaluated the impact of autophagy modulation by different pharmacological/genetic approaches on the viability and phenotype of murine CSCs, which had been subjected to nutrient deprivation or hyperglycemia, in order to mimic relevant stress conditions and risk factors of cardiovascular diseases. Our results show that autophagy is activated in CSCs by nutrient deprivation, and that autophagy induction by trehalose or autophagy-related protein 7 (ATG7)-overexpression can significantly preserve CSC viability. Furthermore, autophagy induction is associated with a higher proportion of primitive, non-activated stem cell antigen 1 (Sca1)-positive cells, and with a reduced fibrotic fraction (positive for the discoidin domain-containing receptor 2, DDR2) in the CSC pool after nutrient deprivation. Hyperglycemia, on the other hand, is associated with reduced autophagic flux in CSCs, and with a significant reduction in primitive Sca1+ cells. Autophagy induction by adenoviral-mediated ATG7-overexpression maintains a cardioprotective, anti-inflammatory and pro-angiogenic paracrine profile of CSCs exposed to hyperglycemia for 1 week. Finally, autophagy induction by ATG7-overexpression during hyperglycemia can significantly preserve cell viability in CSCs, which were subsequently exposed to nutrient deprivation, reducing hyperglycemia-induced impairment of cell resistance to stress. In conclusion, our results show that autophagy stimulation preserves CSC viability and function in response to metabolic stressors, suggesting that it may boost the beneficial functions of CSCs in cardiac repair mechanisms.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The impact of autophagy modulation on phenotype and survival of cardiac stromal cells under metabolic stress

Chimenti

Picchio

Pagano³

et al. 2022

Cell Death Discov.

Self Cite

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“…Therefore, a so-called healthy diet plays a key role in both, primary and secondary cardiovascular prevention, and is given a class I recommendation in current guidelines [ 5 ]. Further, unhealthy diet patterns may have pro-inflammatory properties with the risk of the development and aggravation of inflammatory diseases including pulmonary infections [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Altered nutrition behavior during COVID-19 pandemic lockdown in young adults

et al. 2020

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Purpose The COVID-19 pandemic and the implemented lockdown strongly impact on everyone’s daily life. Stressful situations are known to alter eating habits and increase the risk for obesity. In our study, we aimed to investigate the effect of the lockdown measures on nutrition behavior among young adults. Methods In this cross-sectional study, we enrolled 1964 voluntary participants from Bavarian universities. All participants were asked to complete an online questionnaire, semi-quantitatively evaluating the amount and type of food before and during pandemic lockdown. Study subjects were inquired to give information about acquisition and food procurement. The primary outcome was the change in food amount, secondary outcomes included alterations of food composition and procurement. Results Our study cohort (mean age 23.3 ± 4.0 years, 28.5% male) had a mean body mass index of 22.1 ± 4.5 kg/m2. The overall food amount increased in 31.2% of participants (n = 610) during lockdown and decreased in 16.8% (n = 328). A multinominal regression model revealed that an increased food intake was less likely in male participants (OR, 0.7 [CI 0.6–0.9]) and more likely with increasing BMI (OR, 1.4 [CI 1.3–2.0]), increased sports activity (OR, 1.3 [CI 1.2–1.8]), augmented mental stress (OR 1.4 [1.1–1.7]), and an alteration of alcohol consumption (reduced alcohol amount, OR, 1.4 [CI 1.1–1.7], increased alcohol, OR, 1.9 [CI 1.4–2.5]). Increase in food intake was mainly triggered by consumption of bread (increased in 46.8%, n = 284) and confectionary (increased in 64.4%, n = 389). Conclusion The COVID-19 pandemic lockdown significantly affected eating habits in young adults. Further investigation to evaluate long-term effects on weight change and comorbidities are warranted.

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“…Sustained MMP activation will lead to extracellular matrix remodeling. Fifth, ROS mediate growth responses in ventricular myocytes by stimulating the activity of several growth factors including transforming growth factor-β1 (TGF-β1), [223,224] VEGF, [225] fibroblast growth factor-2 (FGF-2), [226], and PDGF [227]. Sixth, oxidative stress promotes vasoconstriction by increasing the production of endothelin-1 [228] and angiotensin II by increased production of 02-via the NADPH oxidase [229].…”

Section: Oxydative Stressmentioning

confidence: 99%

The Role of Neurohormonal Systems, Inflammatory Mediators and Oxydative Stress in Cardiomyopathy

Zolty¹

2021

Cardiomyopathy - Disease of the Heart Muscle

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Cardiomyopathy and more specifically the dilated cardiomyopathy, regardless of severity, is associated with activation of neuro-hormonal, cytokine and oxidative stress signaling pathways that alter the structure and function of cardiac myocytes and non-myocyte cells. These cellular alterations culminate in the morphological changes in cardiac structure termed as cardiac remodeling, a maladaptive process that contributes to further left ventricular dysfunction and heart failure development. This pathological progression is mainly driven by circulating mediators, in particular angiotensin II and norepinephrine. Natriuretic peptides, endothelin-1, vasopressin play also an important role in the progression of the cardiomyopathy. Cardiac inflammation, mediated by cytokines such as tumor necrosis factor-α (TNF-α), interleukins 1 (IL-1) and 6 (IL-6), as well as the oxidative stress were also shown to worsen the cardiac function. Although these pathways have been described separately, they are critically inter-dependent in the response to the development and progression of the dilated cardiomyopathy. This chapter reviews the cellular basis for cardiac remodeling and the mechanisms that contribute to these cellular abnormalities and, more broadly, to the pathophysiology of dilated cardiomyopathy, its progression and its potential treatments.

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The Microenvironment of Decellularized Extracellular Matrix from Heart Failure Myocardium Alters the Balance between Angiogenic and Fibrotic Signals from Stromal Primitive Cells

Cited by 26 publications

References 63 publications

The impact of autophagy modulation on phenotype and survival of cardiac stromal cells under metabolic stress

The impact of autophagy modulation on phenotype and survival of cardiac stromal cells under metabolic stress

Altered nutrition behavior during COVID-19 pandemic lockdown in young adults

The Role of Neurohormonal Systems, Inflammatory Mediators and Oxydative Stress in Cardiomyopathy

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