Publications by authors named "Marchitti S"
Atrial natriuretic peptide (ANP) modulates stress-induced autophagy in endothelial cells.
Biochim Biophys Acta Mol Cell Res
January 2025
Atrial natriuretic peptide (ANP), a cardiac hormone involved in the regulation of water/sodium balance and blood pressure, is also secreted by endothelial cells, where it exerts protective effects in response to stress. Autophagy is an intracellular self-renewal process involved in the degradation of dysfunctional cytoplasmic elements. ANP was recently reported to act as an extracellular regulator of cardiac autophagy.
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- Heart failure is a serious side effect of doxorubicin (DOX) in cancer patients, and this study investigates the role of the MST1 kinase in DOX-induced heart damage.
- Researchers used mice with normal MST1 and those with a modified version that can't activate (dominant-negative) to analyze the effects of DOX treatment, finding that MST1 activation contributes to heart injury.
- The study concludes that inhibiting MST1 can protect against DOX-induced heart damage by preventing the downregulation of SIRT3, a protective protein, which was also found altered in heart tissue from cancer patients receiving DOX.
Background: A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function.
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- Dkk3 (Dickkopf-3) is a protein that influences blood pressure regulation and is linked to hypertension in rats; its full role in cardiovascular health remains unclear.* -
- Research using genetically modified mice and hypertensive rat models showed that deleting Dkk3 increased blood pressure and impaired blood vessel relaxation, but restoring Dkk3 countered these effects.* -
- The protein functions by enhancing VEGF (vascular endothelial growth factor) expression and activating a signaling pathway that lowers blood pressure, highlighting Dkk3’s potential as a therapeutic target for hypertension.*
Mitochondrial dysfunction, causing increased reactive oxygen species (ROS) production, is a molecular feature of heart failure (HF). A defective antioxidant response and mitophagic flux were reported in circulating leucocytes of patients with chronic HF and reduced ejection fraction (HFrEF). Atrial natriuretic peptide (ANP) exerts many cardiac beneficial effects, including the ability to protect cardiomyocytes by promoting autophagy.
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- * Research showed that high salt significantly damages brain endothelial cells, causing oxidative stress and reduced cell viability.
- * A bergamot polyphenolic fraction (BPF) was found to mitigate these harmful effects, improving cell function and reducing oxidative stress, suggesting it could help treat vascular disorders.
Background: The tricuspid annular plane systolic excursion/systolic pulmonary arterial pressure (TAPSE/sPAP) ratio is an echocardiographic estimation of the right ventricle to pulmonary artery (RV/PA) coupling, with a validated prognostic role in different clinical settings. Systemic sclerosis (SSc) patients without evident cardiovascular involvement frequently display subtle RV impairment. The amino-terminal atrial natriuretic peptide (NT-proANP) plasma level relates to SSc disease progression and mortality.
View Article and Find Full Text PDFTrehalose, spermidine, nicotinamide, and polyphenols have been shown to display pro-autophagic and antioxidant properties, eventually reducing cardiovascular and ischemic complications. This study aimed to investigate whether a mixture of these components improves maximal walking distance (MWD) in peripheral artery disease (PAD) patients. Nitrite/nitrate (NOx), endothelin-1, sNOX2-dp, H2O2 production, H2O2 break-down activity (HBA), ATG5 and P62 levels, flow-mediated dilation (FMD), and MWD were evaluated in 20 PAD patients randomly allocated to 10.
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- - NPPA (atrial natriuretic peptide) plays a significant role in protecting the heart by preventing cell damage, reducing fibrosis, and maintaining blood vessel integrity, but the exact mechanisms behind these benefits are still being studied.
- - The study reveals that NPPA activates autophagy in cardiomyocytes (heart muscle cells) through specific receptors and signaling pathways, and this process helps cells survive stress from conditions like low glucose or lack of oxygen.
- - Research using knockout mice demonstrates that without NPPA, there is greater cell damage during ischemia-reperfusion injury, and enhancing autophagy can reduce this damage, indicating that NPPA is a crucial factor in regulating autophagy in the heart.
Article Synopsis
- Mitochondrial dysfunction, particularly a deficiency in complex I, has been linked to coronary artery disease (CAD) and is implicated in various cardiovascular issues, including acute coronary syndrome (ACS).
- A study involving 260 CAD patients found that the T allele of the /rs23117379 genetic variant is associated with an earlier onset of ACS and a higher risk of recurrence.
- The findings suggest that this genetic variant may serve as a potential risk factor for cardiovascular diseases due to its role in mitochondrial dysfunction.
The mitochondrial uncoupling protein 2 (UCP2) acts as an anion transporter and as an antioxidant factor able to reduce the reactive oxygen species level. Based on its effects, UCP2 prevents the membrane lipids, proteins, and DNA damage while preserving normal cellular functions. Many variants have been identified within the human .
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- There is a lack of comprehensive data on PFAS concentrations in breast milk among women in the U.S. and Canada, despite 20 years of biomonitoring studies on PFAS in serum and urine.
- The study aims to document existing breast milk PFAS concentrations, estimate levels based on maternal serum, and compare these concentrations to children's drinking water safety values.
- Findings show that measured and estimated levels of PFOA and PFOS in breast milk often exceed safe drinking water limits for children, while PFHxS and PFNA levels are generally below these limits, though estimates can vary significantly.
Article Synopsis
- Stroke is a leading cause of death and disability globally, prompting research into biological factors that contribute to its onset, particularly mitochondrial dysfunction, autophagy, and calcium regulation in cells.
- The study highlights the role of store-operated calcium entry (SOCE) mechanisms, specifically how mutations in the calcium sensor STIM1 affect calcium levels, potentially worsening stroke effects in certain rat strains.
- The article emphasizes STIM1's significance in experimental stroke research, linking it to stroke vulnerability and discussing future clinical implications for human treatments.
Article Synopsis
- UCP2 is crucial for protecting against vascular diseases linked to high salt intake, as shown in various animal models and human studies.
- Reducing UCP2 levels worsens vascular health and increases damage in models prone to stroke, while increasing UCP2 levels helps mitigate these harmful effects.
- UCP2 promotes autophagy and mitophagy in response to high salt and oxidative stress, which helps maintain cell viability; when UCP2 is silenced, these protective processes are disrupted, but introducing an autophagy inducer can reverse some damage.
We utilized a practical, transparent approach for systematically reviewing a chemical-specific evidence base. This approach was used for a case study of ozone inhalation exposure and adverse metabolic effects (overweight/obesity, Type 1 diabetes [T1D], Type 2 diabetes [T2D], and metabolic syndrome). We followed the basic principles of systematic review.
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- Cerebrovascular disease is a big health problem caused by high blood pressure, and new ways to treat it are needed.
- A sugar called trehalose (TRE) showed promise in helping prevent strokes in rats that were prone to them while eating a high-salt diet.
- TRE helped reduce strokes and kidney damage, lowered blood pressure, and improved brain and cell functions by activating a process that clears out damaged parts of cells.
Article Synopsis
- Sphingolipids, key molecules in cell membranes affecting blood vessel health, are linked to various vascular disorders but their role in hypertension-related brain and kidney damage is unclear.
- This study compared sphingolipid metabolism in hypertensive rat strains (SHRSP and SHRSR) with normotensive rats (WKY) and found significant metabolic alterations in both the brain and kidneys of hypertensive rats.
- Specific issues, like reduced enzyme expression related to sphingosine-1-phosphate metabolism, were unique to the SHRSP strain, indicating potential pathways for future research and therapies targeting hypertension-related organ damage.
Article Synopsis
- Uncoupling protein 2 (UCP2) is a mitochondrial protein that regulates processes such as mitochondrial membrane potential, reactive oxygen species production, and calcium balance, with expression influenced by genetic, transcriptional, and post-translational factors.
- Activation of UCP2 through the AMPK/PPAR-α pathway has been shown to protect against renal damage and stroke in animal studies, and UCP2 is crucial in the context of heart diseases and metabolic disorders like obesity and diabetes.
- Genetic variants of UCP2 in humans are linked to a higher risk of type 2 diabetes and ischemic stroke, while various natural compounds and clinical drugs can modulate UCP2 levels, highlighting its potential for treating multiple health
Background And Purpose: Oxidative stress and insufficient autophagy activity are associated with inflammatory processes and are common features of many cardiovascular diseases (CVDs). We investigated if a combination of natural activators of autophagy could modulate oxidative stress, platelet aggregation and endothelial cell survival and function in response to stress.
Experimental Approach: Ex vivo platelet aggregation and activation, H O production and autophagy were measured in platelets of subjects at high cardiovascular risk, including smokers, patients with metabolic syndrome (MetS) and patients with atrial fibrillation (AF).
Background The role of microRNAs dysregulation in tobacco cigarette smoking-induced vascular damage still needs to be clarified. We assessed the acute effects of tobacco cigarette smoking on endothelial cell-related circulating microRNAs in healthy subjects. In addition, we investigated the potential role of microRNAs in smoking-dependent endothelial cell damage.
View Article and Find Full Text PDFBackground And Aim: Although hypertension guidelines highlight the benefits of achieving the recommended blood pressure (BP) targets, hypertension control rate is still insufficient, mostly in high or very high cardiovascular (CV) risk patients. Thus, we aimed to estimate BP control in a cohort of patients at high CV risk in both primary and secondary prevention.
Methods And Results: A single-center, cross-sectional study was conducted by extracting data from a medical database of adult outpatients aged 40-75 years, who were referred to our Hypertension Unit, Rome (IT), for hypertension assessment.
Article Synopsis
- Stroke is a major cause of death and disability, and its pathogenesis involves complex inflammatory and immune responses that damage brain tissue initially but can later aid in repair.
- Damage-associated molecular patterns (DAMPs) play a crucial role in exacerbating brain injury by disrupting the blood-brain barrier and promoting inflammation, while regulatory T lymphocytes (Tregs) can have protective effects.
- Understanding these processes is essential for developing new therapies, though translating research findings from animal models to human treatment remains challenging and requires more investigation.
Article Synopsis
- The study investigates the impact of the T2238C variant of the ANP gene on cardiovascular events (CVEs) in patients with atrial fibrillation (AF) who are on anticoagulation therapy.
- It analyzed 557 patients from the ATHERO-AF cohort, classifying them into wild type, heterozygous, and homozygous variants to assess the frequency of CVEs like stroke and myocardial infarction.
- Results showed that patients with the homozygous C2238 allele had a significantly higher risk for CVEs, confirming this variant as a potential risk factor for these cardiovascular complications in AF patients.
Article Synopsis
- Downregulation of uncoupling protein-2 (UCP2) leads to more brain and kidney issues in stroke-prone rats on a hypersodic diet, but overexpression of UCP2 can help reduce this organ damage.
- Brain-specific UCP2 overexpression in these rats resulted in delayed stroke onset and less kidney damage, despite unchanged blood pressure.
- The study indicates that UCP2 may enhance mitochondrial function and lower oxidative damage and inflammation, suggesting potential treatments focused on boosting UCP2 for mitigating hypertension-related organ damage.