Claudio T De Souza

Dr. Claudio T De Souza


Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2019 in Redox Report
Verified
Journal Article
Open access
AMAna Lucia Bernardo Carvalho Morsch
Ana Lucia Bernardo Carvalho Morsch
EWElvis Wisniewski
Elvis Wisniewski
TLThais Fernandes Luciano
Thais Fernandes Luciano
VCVitor Hugo Comin
Vitor Hugo Comin
GSGustavo de Bem Silveira
Gustavo de Bem Silveira
CSClaudio T De Souza
Claudio T De Souza
Many pathological conditions linked to cigarette smoking are caused by the production of reactive oxygen species (ROS). The present study was conducted to analyze the effect of ROS on the lungs of Swiss mice exposed to cigarette smoking, focusing on autophagy-mediated mechanisms, and investigate the involvement of SESN2, AMPK, and mTOR signaling. Mice were exposed to cigarette smoke (CS) for 7, 15, 30, 45, and 60 days; the control group was not exposed to CS. Only mice exposed to CS for 45 days were selected for subsequent N-acetylcysteine (NAC) supplementation and smoke cessation analyses. Exposure to CS increased the production of ROS and induced molecular changes in the autophagy pathway, including an increase in phosphorylated AMPK and ULK1, reduction in phosphorylated mTOR, and increases in SESN2, ATG12, and LC3B levels. NAC supplementation reduced ROS levels and reversed all molecular changes observed upon CS treatment, suggesting the involvement of oxidative stress in inducing autophagy upon CS exposure. When exposure to CS was stopped, there were decreases in the levels of oxidative stress, AMPK and ULK1 phosphorylation, and autophagy-initiating molecules and increase in mTOR phosphorylation. In conclusion, these results suggest the involvement of ROS, SESN2, AMPK, and mTOR in the CS-induced autophagic process in the lung.

9 August 2024 in Metabolic Brain Disease
Verified
Journal Article
Closed access
PDF file
TLThaís Fernandes Luciano
Thaís Fernandes Luciano
CSClaudio T De Souza
Claudio T De Souza
JOJade de Oliveira
Jade de Oliveira
AMAlexandre Pastoris Muller
Alexandre Pastoris Muller

17 August 2025 in Revista ft
Verified
Journal Article
Closed access
WNWellington Henrique Justo Neto
Wellington Henrique Justo Neto
MLMário Flávio Cardoso de Lima
Mário Flávio Cardoso de Lima
MLMarina Guedes Fraga Lopes
Marina Guedes Fraga Lopes
SLSheila Cristina Potente Dutra Luquetti
Sheila Cristina Potente Dutra Luquetti
CSClaudio T De Souza
Claudio T De Souza
Introduction and Objective: Some impacts of obesity are still not fully understood, such as mitochondrial dysfunction. The significance of mitochondria in regulating processes like oxidative balance, insulin signaling, inflammatory response, and apoptosis is well recognized. Restoring mitochondrial function is pivotal in treating obesity and its complications. A therapeutic target is irisin, a hormone known to regulate mitochondrial function and potentially influenced by omega-3 fatty acid consumption. This review aimed to assess the effects of omega-3 supplementation on mitochondrial dysfunction in overweight individuals. Materials and Methods: A systematic review was conducted using articles sourced from databases including Medline, Cochrane, Embase, BVS, and Opengrey. The PICO strategy was adopted to establish eligibility criteria. Results: A total of 4 studies met the eligibility criteria and were explored to form the review. Discussion: Alterations induced by omega-3 consumption impact crucial events regulated by mitochondria, resulting in reduced oxidative and inflammatory damage, improved control of apoptotic pathways, and enhanced metabolism of substrates such as fats and carbohydrates, involving adjustments in insulin signaling. Conclusion: Omega-3 supplementation yields beneficial effects on mitochondrial dysfunction in overweight patients, influencing responses like chronic inflammation, oxidative balance, insulin sensitivity, and apoptosis.

22 September 2025 in Revista ft
Verified
Journal Article
Closed access
BPBárbara Loures Peralva
Bárbara Loures Peralva
MLMário Flávio Cardoso de Lima
Mário Flávio Cardoso de Lima
KSKelli Borges dos Santos
Kelli Borges dos Santos
MLMarina Guedes Fraga Lopes
Marina Guedes Fraga Lopes
CSClaudio T De Souza
Claudio T De Souza
Aims: The present study aimed to synthesize the literature on the efficacy of treatments with a positive impact on reducing albuminuria in adult patients with metabolic syndrome (MetS). Methods: The present study followed the Joanna Briggs Institute (JBI) methodology for systematic reviews and meta-analyses. The inclusion criteria were studies evaluating treatments in adult patients with MetS. Studies describing treatments in children, pregnant women, animals and patients with type 1 diabetes were excluded. The databases selected for the search strategy were Cochrane, Embase, Scopus, Medline/PubMed and Dart-E Europe ETheses, without language restrictions. Studies since 2009 were included due to the consensus definition of MetS. Study selection and evaluation and data collection were performed by two independent reviewers. The search strategy was performed in August and September 2021. Results: Twenty-one articles were included, which showed that lifestyle changes and bariatric surgery seemed to reduce albuminuria in patients with MetS. Only three articles were included in the meta-analysis. In this analysis, diet alone or together with physical exercise was effective for reducing albuminuria in patients with MetS. Conclusions: Diet alone or associated with physical exercise has an impact on decreasing albuminuria in patients with MetS.