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  1. Article: Commentary: Urinary Neopterin, a New Marker of the Neuroinflammatory Status in Amyotrophic Lateral Sclerosis.

    Espíndola, Gisele / Scheffer, Débora da Luz / Latini, Alexandra

    Frontiers in neuroscience

    2021  Volume 15, Page(s) 645694

    Language English
    Publishing date 2021-03-23
    Publishing country Switzerland
    Document type Journal Article ; Comment
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2021.645694
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Exercise-induced immune system response: Anti-inflammatory status on peripheral and central organs.

    Scheffer, Débora da Luz / Latini, Alexandra

    Biochimica et biophysica acta. Molecular basis of disease

    2020  Volume 1866, Issue 10, Page(s) 165823

    Abstract: A wide array of molecular pathways has been investigated during the past decade in order to understand the mechanisms by which the practice of physical exercise promotes neuroprotection and reduces the risk of developing communicable and non-communicable ...

    Abstract A wide array of molecular pathways has been investigated during the past decade in order to understand the mechanisms by which the practice of physical exercise promotes neuroprotection and reduces the risk of developing communicable and non-communicable chronic diseases. While a single session of physical exercise may represent a challenge for cell homeostasis, repeated physical exercise sessions will improve immunosurveillance and immunocompetence. Additionally, immune cells from the central nervous system will acquire an anti-inflammatory phenotype, protecting central functions from age-induced cognitive decline. This review highlights the exercise-induced anti-inflammatory effect on the prevention or treatment of common chronic clinical and experimental settings. It also suggests the use of pterins in biological fluids as sensitive biomarkers to follow the anti-inflammatory effect of physical exercise.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Biomarkers ; Blood-Brain Barrier/immunology ; Chronic Disease ; Communicable Diseases/immunology ; Cytokines ; Databases, Factual ; Exercise/physiology ; Humans ; Immune System/drug effects ; Immune System/immunology ; Immunity, Innate/immunology ; Inflammation/immunology ; Neopterin/pharmacology ; Neuroprotection/immunology
    Chemical Substances Anti-Inflammatory Agents ; Biomarkers ; Cytokines ; Neopterin (670-65-5)
    Keywords covid19
    Language English
    Publishing date 2020-04-29
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2020.165823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mitochondrial Fusion, Fission, and Mitophagy in Cardiac Diseases: Challenges and Therapeutic Opportunities.

    Scheffer, Débora da Luz / Garcia, Adriana Ann / Lee, Lucia / Mochly-Rosen, Daria / Ferreira, Julio Cesar Batista

    Antioxidants & redox signaling

    2022  Volume 36, Issue 13-15, Page(s) 844–863

    Abstract: Significance: ...

    Abstract Significance:
    MeSH term(s) Heart Failure/metabolism ; Humans ; Mitochondria/metabolism ; Mitochondrial Dynamics ; Mitophagy ; Myocardial Infarction/metabolism
    Language English
    Publishing date 2022-04-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2021.0145
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Exercise-induced immune system response: Anti-inflammatory status on peripheral and central organs

    Scheffer, Débora da Luz / Latini, Alexandra

    Biochim Biophys Acta Mol Basis Dis

    Abstract: A wide array of molecular pathways has been investigated during the past decade in order to understand the mechanisms by which the practice of physical exercise promotes neuroprotection and reduces the risk of developing communicable and non-communicable ...

    Abstract A wide array of molecular pathways has been investigated during the past decade in order to understand the mechanisms by which the practice of physical exercise promotes neuroprotection and reduces the risk of developing communicable and non-communicable chronic diseases. While a single session of physical exercise may represent a challenge for cell homeostasis, repeated physical exercise sessions will improve immunosurveillance and immunocompetence. Additionally, immune cells from the central nervous system will acquire an anti-inflammatory phenotype, protecting central functions from age-induced cognitive decline. This review highlights the exercise-induced anti-inflammatory effect on the prevention or treatment of common chronic clinical and experimental settings. It also suggests the use of pterins in biological fluids as sensitive biomarkers to follow the anti-inflammatory effect of physical exercise.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #133265
    Database COVID19

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  5. Article ; Online: Muscle-specific ER-associated degradation maintains postnatal muscle hypertrophy and systemic energy metabolism.

    Abdon, Benedict / Liang, Yusheng / da Luz Scheffer, Débora / Torres, Mauricio / Shrestha, Neha / Reinert, Rachel B / Lu, You / Pederson, Brent / Bugarin-Lapuz, Amara / Kersten, Sander / Qi, Ling

    JCI insight

    2023  Volume 8, Issue 17

    Abstract: The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated ... ...

    Abstract The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
    MeSH term(s) Humans ; Endoplasmic Reticulum-Associated Degradation ; Ubiquitin-Protein Ligases/metabolism ; Proteins/genetics ; Muscles/metabolism ; Energy Metabolism ; Hypertrophy/metabolism
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proteins ; SEL1L protein, human
    Language English
    Publishing date 2023-08-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.170387
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Physical-Exercise-Induced Antioxidant Effects on the Brain and Skeletal Muscle.

    Souza, Jennyffer / da Silva, Rodrigo Augusto / da Luz Scheffer, Débora / Penteado, Rafael / Solano, Alexandre / Barros, Leonardo / Budde, Henning / Trostchansky, Andrés / Latini, Alexandra

    Antioxidants (Basel, Switzerland)

    2022  Volume 11, Issue 5

    Abstract: Erythroid-related nuclear factor 2 (NRF2) and the antioxidant-responsive-elements (ARE) signaling pathway are the master regulators of cell antioxidant defenses, playing a key role in maintaining cellular homeostasis, a scenario in which proper ... ...

    Abstract Erythroid-related nuclear factor 2 (NRF2) and the antioxidant-responsive-elements (ARE) signaling pathway are the master regulators of cell antioxidant defenses, playing a key role in maintaining cellular homeostasis, a scenario in which proper mitochondrial function is essential. Increasing evidence indicates that the regular practice of physical exercise increases cellular antioxidant defenses by activating NRF2 signaling. This manuscript reviewed classic and ongoing research on the beneficial effects of exercise on the antioxidant system in both the brain and skeletal muscle.
    Language English
    Publishing date 2022-04-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11050826
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Muscle Fatigue Is Attenuated When Applying Intermittent Compared With Continuous Blood Flow Restriction During Endurance Cycling.

    Corvino, Rogério Bulhões / Scheffer, Débora da Luz / Penteado Dos Santos, Rafael / Latini, Alexandra / Oliveira, Anderson Souza / Caputo, Fabrizio

    International journal of sports physiology and performance

    2022  Volume 17, Issue 7, Page(s) 1126–1131

    Abstract: Purpose: The aim of this study was to identify a blood-flow-restriction (BFR) endurance exercise protocol that maximizes metabolic strain and minimizes muscle fatigue.: Methods: Twelve healthy participants accomplished 5 different interval cycling ... ...

    Abstract Purpose: The aim of this study was to identify a blood-flow-restriction (BFR) endurance exercise protocol that maximizes metabolic strain and minimizes muscle fatigue.
    Methods: Twelve healthy participants accomplished 5 different interval cycling endurance exercises (2-min work, 1-min rest) in a randomized order: (1) control, low intensity with unrestricted blood flow (CON30); (2) low intensity with intermittent BFR (i-BFR30, ∼150 mm Hg); (3) low intensity with continuous BFR (c-BFR, ∼100 mm Hg); (4) unloaded cycling with i-BFR0 (∼150 mm Hg); and (5) high intensity (HI) with unrestricted blood flow. Force production, creatine kinase activity, antioxidant markers, blood pH, and potassium (K+) were measured in a range of 5 minutes before and after each cycling exercise protocol.
    Results: HI showed the highest reduction (Δ = -0.26 [0.05], d = 5.6) on blood pH. Delta pH for c-BRF30 (Δ = -0.02 [0.03], d = 0.8) and Δ pH for i-BRF30 (Δ = -0.04 [0.03], d = 1.6) were different from each other, and both were higher compared with CON30 (Δ = 0.03 [0.03]). There was significant before-to-after force loss following HI (Δ = 55 [40] N·m-1, d = 1.5) and c-BFR30 (Δ = 27 [21] N·m-1, d = 0.7) protocols only, which were accompanied by significant increases in K+ (HI: Δ = 0.94 [0.65] mmol·L-1, d = 1.8; c-BFR30: Δ = 0.72 [0.85] mmol·L-1, d = 1.2). Moreover, all BFR conditions elicited slight increases in plasma creatine kinase, but not for HI and CON30. Glutathione changes from before to after were significant for all BFR conditions and HI, but not for CON30.
    Conclusions: The attenuation in fatigue-induced reductions in maximal force suggests that i-BFR exercise could be preferable to c-BFR in improving exercise capacity, with considerably less biologic stress elicited from HI exercises.
    MeSH term(s) Creatine Kinase/metabolism ; Humans ; Muscle Fatigue ; Muscle, Skeletal/physiology ; Regional Blood Flow/physiology ; Resistance Training/methods
    Chemical Substances Creatine Kinase (EC 2.7.3.2)
    Language English
    Publishing date 2022-05-12
    Publishing country United States
    Document type Journal Article
    ISSN 1555-0273
    ISSN (online) 1555-0273
    DOI 10.1123/ijspp.2021-0523
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Muscle-specific ER-associated degradation maintains postnatal muscle hypertrophy and systemic energy metabolism

    Benedict Abdon / Yusheng Liang / Débora da Luz Scheffer / Mauricio Torres / Neha Shrestha / Rachel B. Reinert / You Lu / Brent Pederson / Amara Bugarin-Lapuz / Sander Kersten / Ling Qi

    JCI Insight, Vol 8, Iss

    2023  Volume 17

    Abstract: The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated ... ...

    Abstract The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
    Keywords Cell biology ; Muscle biology ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2023-09-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Moderate running exercise prevents excessive immune system activation.

    Scheffer, Débora da Luz / Ghisoni, Karina / Aguiar, Aderbal Silva / Latini, Alexandra

    Physiology & behavior

    2019  Volume 204, Page(s) 248–255

    Abstract: Benefits of exercise have been documented for many diseases with a chronic progression, including obesity, diabetes mellitus, cardiovascular diseases, neurodegenerative diseases, certain types of cancers, and overall mortality. Low-grade systemic ... ...

    Abstract Benefits of exercise have been documented for many diseases with a chronic progression, including obesity, diabetes mellitus, cardiovascular diseases, neurodegenerative diseases, certain types of cancers, and overall mortality. Low-grade systemic inflammation is a key component of these pathologies and it has been demonstrated that can be prevented by performing regularly physical exercise. The aim of this study was to examine the effect of lipopolysaccharide (LPS)-induced inflammation on glucose and insulin tolerance, exercise performance, production of urinary neopterin and striatal neurotransmitters levels in adult male C57BL/6 mice. Increased blood glucose clearance and insulin sensitivity were observed after a single administration of glucose (2 g/kg, p.o.) or insulin (0.5 U/kg, i.p.). However, the repeated injection of LPS (0.33 mg/kg/day, i.p.) decreased glucose tolerance and increase urinary neopterin levels, pointing to systemic inflammation. In parallel to the urinary-increased neopterin, it was observed a significant reduction in the striatal dopamine levels and an increase in the serotonin/dopamine ratio. While a single LPS injection (0.33 mg/kg, i.p.) showed impaired performance in the incremental loading test (10 m/min, with 2 m/min increment every 3 min, at 9% grade), a moderate physical exercise protocol (treadmill for three weeks; 5 sessions/week; up to 50 min/day) prevented the exacerbation of immune system activation and preserved mitochondrial activity in skeletal muscle from mice with continuous LPS infusion (infusion pumps: 0.83 mg/kg/day, i.p.). In conclusion, the peripheral-induced inflammation elicited metabolic alterations that provoked impairment in striatal dopamine metabolism. The moderate exercise prevented the increase of urinary neopterin and preserved mitochondrial activity under LPS-induced inflammatory conditions.
    MeSH term(s) Animals ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Inflammation/metabolism ; Insulin Resistance/physiology ; Lipopolysaccharides/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Neopterin/urine ; Physical Conditioning, Animal/physiology ; Running/physiology ; Serotonin/metabolism
    Chemical Substances Lipopolysaccharides ; Serotonin (333DO1RDJY) ; Neopterin (670-65-5) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2019-02-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3907-x
    ISSN 1873-507X ; 0031-9384
    ISSN (online) 1873-507X
    ISSN 0031-9384
    DOI 10.1016/j.physbeh.2019.02.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Muscle-specific ER-associated degradation maintains postnatal muscle hypertrophy and systemic energy metabolism

    Abdon, Benedict / Liang, Yusheng / da Luz Scheffer, Débora / Torres, Mauricio / Shrestha, Neha / Reinert, Rachel / Lu, You / Pederson, Brent / Bugarin-Lapuz, Amara / Kersten, Sander / Qi, Ling

    JCI Insight

    2023  Volume 8, Issue 17

    Abstract: The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated ... ...

    Abstract The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
    Keywords Life Science
    Subject code 610
    Language English
    Publishing country nl
    Document type Article ; Online
    ISSN 2379-3708
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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