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Article ; Online: Implications of mitochondrial fusion and fission in skeletal muscle mass and health.

Romanello, Vanina / Sandri, Marco

Seminars in cell & developmental biology

2022 Volume 143, Page(s) 46–53

Abstract: The continuous dynamic reshaping of mitochondria by fusion and fission events is critical to keep mitochondrial quality and function under control in response to changes in energy and stress. Maintaining a functional, highly interconnected mitochondrial ... ...

Abstract	The continuous dynamic reshaping of mitochondria by fusion and fission events is critical to keep mitochondrial quality and function under control in response to changes in energy and stress. Maintaining a functional, highly interconnected mitochondrial reticulum ensures rapid energy production and distribution. Moreover, mitochondrial networks act as dynamic signaling hub to adapt to the metabolic demands imposed by contraction, energy expenditure, and general metabolism. However, excessive mitochondrial fusion or fission results in the disruption of the skeletal muscle mitochondrial network integrity and activates a retrograde response from mitochondria to the nucleus, leading to muscle atrophy, weakness and influencing whole-body homeostasis. These actions are mediated via the secretion of mitochondrial-stress myokines such as FGF21 and GDF15. Here we will summarize recent discoveries in the role of mitochondrial fusion and fission in the control of muscle mass and in regulating physiological homeostasis and disease progression.
MeSH term(s)	Mitochondrial Dynamics ; Muscle, Skeletal/metabolism ; Mitochondria, Muscle/physiology ; Humans
Language	English
Publishing date	2022-02-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2022.02.011
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Article ; Online: Anabolic Resistance in the Pathogenesis of Sarcopenia in the Elderly: Role of Nutrition and Exercise in Young and Old People.

Tezze, Caterina / Sandri, Marco / Tessari, Paolo

Nutrients

2023 Volume 15, Issue 18

Abstract: The development of sarcopenia in the elderly is associated with many potential factors and/or processes that impair the renovation and maintenance of skeletal muscle mass and strength as ageing progresses. Among them, a defect by skeletal muscle to ... ...

Abstract	The development of sarcopenia in the elderly is associated with many potential factors and/or processes that impair the renovation and maintenance of skeletal muscle mass and strength as ageing progresses. Among them, a defect by skeletal muscle to respond to anabolic stimuli is to be considered. Common anabolic stimuli/signals in skeletal muscle are hormones (insulin, growth hormones, IGF-1, androgens, and β-agonists such epinephrine), substrates (amino acids such as protein precursors on top, but also glucose and fat, as source of energy), metabolites (such as β-agonists and HMB), various biochemical/intracellular mediators), physical exercise, neurogenic and immune-modulating factors, etc. Each of them may exhibit a reduced effect upon skeletal muscle in ageing. In this article, we overview the role of anabolic signals on muscle metabolism, as well as currently available evidence of resistance, at the skeletal muscle level, to anabolic factors, from both in vitro and in vivo studies. Some indications on how to augment the effects of anabolic signals on skeletal muscle are provided.
MeSH term(s)	Humans ; Aged ; Sarcopenia ; Muscle, Skeletal ; Nutritional Status ; Exercise ; Insulin
Chemical Substances	Insulin
Language	English
Publishing date	2023-09-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15184073
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Article ; Online: Role of autophagy in muscle disease.

Franco-Romero, Anais / Sandri, Marco

Molecular aspects of medicine

2021 Volume 82, Page(s) 101041

Abstract: Beside inherited muscle diseases many catabolic conditions such as insulin resistance, malnutrition, cancer growth, aging, infections, chronic inflammatory status, inactivity, obesity are characterized by loss of muscle mass, strength and function. The ... ...

Abstract	Beside inherited muscle diseases many catabolic conditions such as insulin resistance, malnutrition, cancer growth, aging, infections, chronic inflammatory status, inactivity, obesity are characterized by loss of muscle mass, strength and function. The decrease of muscle quality and quantity increases morbidity, mortality and has a major impact on the quality of life. One of the pathogenetic mechanisms of muscle wasting is the dysregulation of the main protein and organelles quality control system of the cell: the autophagy-lysosome. This review will focus on the role of the autophagy-lysosome system in the different conditions of muscle loss. We will also dissect the signalling pathways that are involved in excessive or defective autophagy regulation. Finally, the state of the art of autophagy modulators that have been used in preclinical or clinical studies to ameliorate muscle mass will be also described.
MeSH term(s)	Autophagy ; Humans ; Lysosomes ; Muscle, Skeletal/pathology ; Muscular Atrophy/pathology ; Quality of Life
Language	English
Publishing date	2021-10-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	197640-0
ISSN	1872-9452 ; 0098-2997
ISSN (online)	1872-9452
ISSN	0098-2997
DOI	10.1016/j.mam.2021.101041
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Article ; Online: Protein breakdown in cancer cachexia.

Sandri, Marco

Seminars in cell & developmental biology

2016 Volume 54, Page(s) 11–19

Abstract: Skeletal muscle is a highly adaptive tissue, capable of altering muscle fiber size, functional capacity and metabolism in response to physiological stimuli. However, pathological conditions such as cancer growth compromise the mechanisms that regulate ... ...

Abstract	Skeletal muscle is a highly adaptive tissue, capable of altering muscle fiber size, functional capacity and metabolism in response to physiological stimuli. However, pathological conditions such as cancer growth compromise the mechanisms that regulate muscle homeostasis, resulting in loss of muscle mass, functional impairment and compromised metabolism. This tumor-induced condition is characterized by enhanced muscle protein breakdown and amino acids release that sustain liver gluconeogenesis and tissue protein synthesis. Proteolysis is controlled by the two most important cellular degradation systems, the ubiquitin proteasome and autophagy lysosome. These systems are carefully regulated by different signalling pathways that determine protein and organelle turnover. In this review we will describe the involvement of the ubiquitin proteasome and autophagy lysosome systems in cancer cachexia and the principal signalling pathways that regulate tumor-induced protein breakdown in muscle.
Language	English
Publishing date	2016-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2015.11.002
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Article ; Online: Memory or amnesia: the dilemma of stem cell therapy in muscular dystrophies.

Sandri, Marco

The Journal of clinical investigation

2015 Volume 125, Issue 12, Page(s) 4331–4333

Abstract: Muscular dystrophies are monogenetic diseases that are often characterized by the degeneration of both cardiac and skeletal muscle. Gene therapy to correct the mutated gene has shown promise in both animal models and clinical trials; however, current ... ...

Abstract	Muscular dystrophies are monogenetic diseases that are often characterized by the degeneration of both cardiac and skeletal muscle. Gene therapy to correct the mutated gene has shown promise in both animal models and clinical trials; however, current gene delivery strategies are limited to the introduction of the corrected gene into only one tissue. Strategies to target multiple striated muscle types would provide a much-needed improvement for the treatment of muscular dystrophies. In this issue of the JCI, Quattrocelli and colleagues demonstrate that induced pluripotent stem cells (iPSCs) with a myogenic propensity are able to engraft into both cardiac and skeletal muscles. The authors also identified a novel pool of mesodermal iPSC-derived progenitors (MiPs). Moreover, the authors show that these MiPs are amenable to gene correction and can restore function in murine dystrophic models. Together, the results of this study provide an important advance in improving gene delivery to treat patients with muscular dystrophy.
MeSH term(s)	Animals ; Cell Differentiation ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mesoderm/metabolism ; Muscle, Skeletal/physiology ; Myocardium ; Regeneration
Language	English
Publishing date	2015-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI85002
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Article: Spatial performance analysis in basketball with CART, random forest and extremely randomized trees.

Zuccolotto, Paola / Sandri, Marco / Manisera, Marica

Annals of operations research

2022 Volume 325, Issue 1, Page(s) 495–519

Abstract: This paper proposes tools for spatial performance analysis in basketball. In detail, we aim at representing maps of the court visualizing areas with different levels of scoring probability of the analysed player or team. To do that, we propose the ... ...

Abstract	This paper proposes tools for spatial performance analysis in basketball. In detail, we aim at representing maps of the court visualizing areas with different levels of scoring probability of the analysed player or team. To do that, we propose the adoption of algorithmic modeling techniques. Firstly, following previous studies, we examine CART, highlighting strengths and weaknesses. With respect to what done in the past, here we propose the use of polar coordinates, which are more consistent with the basketball court geometry. In order to overcome CART's drawbacks while maintaining its points of force, we propose to resort to CART-based ensemble learning algorithms, namely to Random Forest and Extremely Randomized Trees, which are shown to be able to give excellent results in terms of interpretation and robustness. Finally, an index is defined in order to measure the map's graphical goodness, which can be used-jointly with measures of the out-of-sample error-to tune the algorithm's parameters. The functioning of the proposed approaches is shown by the analysis of real data of the NBA regular season 2020/2021.
Language	English
Publishing date	2022-06-03
Publishing country	United States
Document type	Journal Article
ISSN	0254-5330
ISSN	0254-5330
DOI	10.1007/s10479-022-04784-3
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Article ; Online: Signaling Pathways That Control Muscle Mass.

Vainshtein, Anna / Sandri, Marco

International journal of molecular sciences

2020 Volume 21, Issue 13

Abstract: The loss of skeletal muscle mass under a wide range of acute and chronic maladies is associated with poor prognosis, reduced quality of life, and increased mortality. Decades of research indicate the importance of skeletal muscle for whole body ... ...

Abstract	The loss of skeletal muscle mass under a wide range of acute and chronic maladies is associated with poor prognosis, reduced quality of life, and increased mortality. Decades of research indicate the importance of skeletal muscle for whole body metabolism, glucose homeostasis, as well as overall health and wellbeing. This tissue's remarkable ability to rapidly and effectively adapt to changing environmental cues is a double-edged sword. Physiological adaptations that are beneficial throughout life become maladaptive during atrophic conditions. The atrophic program can be activated by mechanical, oxidative, and energetic distress, and is influenced by the availability of nutrients, growth factors, and cytokines. Largely governed by a transcription-dependent mechanism, this program impinges on multiple protein networks including various organelles as well as biosynthetic and quality control systems. Although modulating muscle function to prevent and treat disease is an enticing concept that has intrigued research teams for decades, a lack of thorough understanding of the molecular mechanisms and signaling pathways that control muscle mass, in addition to poor transferability of findings from rodents to humans, has obstructed efforts to develop effective treatments. Here, we review the progress made in unraveling the molecular mechanisms responsible for the regulation of muscle mass, as this continues to be an intensive area of research.
MeSH term(s)	Animals ; Cytokines/metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiology ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Nutrients/metabolism ; Quality of Life ; Signal Transduction/physiology
Chemical Substances	Cytokines ; Intercellular Signaling Peptides and Proteins
Language	English
Publishing date	2020-07-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21134759
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Article ; Online: The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass.

Romanello, Vanina / Sandri, Marco

Cellular and molecular life sciences : CMLS

2020 Volume 78, Issue 4, Page(s) 1305–1328

Abstract: The dynamic coordination of processes controlling the quality of the mitochondrial network is crucial to maintain the function of mitochondria in skeletal muscle. Changes of mitochondrial proteolytic system, dynamics (fusion/fission), and mitophagy ... ...

Abstract	The dynamic coordination of processes controlling the quality of the mitochondrial network is crucial to maintain the function of mitochondria in skeletal muscle. Changes of mitochondrial proteolytic system, dynamics (fusion/fission), and mitophagy induce pathways that affect muscle mass and performance. When muscle mass is lost, the risk of disease onset and premature death is dramatically increased. For instance, poor quality of muscles correlates with the onset progression of several age-related disorders such as diabetes, obesity, cancer, and aging sarcopenia. To date, there are no drug therapies to reverse muscle loss, and exercise remains the best approach to improve mitochondrial health and to slow atrophy in several diseases. This review will describe the principal mechanisms that control mitochondrial quality and the pathways that link mitochondrial dysfunction to muscle mass regulation.
MeSH term(s)	Aging/genetics ; Aging/pathology ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Dynamics/genetics ; Mitophagy/genetics ; Muscle, Skeletal/growth & development ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Diseases/genetics ; Muscular Diseases/metabolism ; Muscular Diseases/pathology ; Proteolysis
Language	English
Publishing date	2020-10-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-020-03662-0
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Article ; Online: Regulation and involvement of the ubiquitin ligases in muscle atrophy.

Sandri, Marco

Free radical biology & medicine

2014 Volume 75 Suppl 1, Page(s) S4

Abstract: The ability to activate compensatory mechanisms in response to environmental stress is an important factor for survival and maintenance of cellular functions. A system that is often activated both in short and prolonged stress conditions is ubiquitin ... ...

Abstract	The ability to activate compensatory mechanisms in response to environmental stress is an important factor for survival and maintenance of cellular functions. A system that is often activated both in short and prolonged stress conditions is ubiquitin proteasome system (UPS). UPS is required to clear the cell from dysfunctional and altered proteins and is reported to increase during catabolic conditions. This increase contributes to the loss of contractile proteins and, when is exacerbated, to cachexia. Here I'll present the last data about UPS regulation, the role of UPS in protein turnover in skeletal muscles and the pathogenetic implications of deregulated UPS in muscle disorders.
Language	English
Publishing date	2014-12-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2014.10.833
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Article ; Online: Age-Related In Vivo Structural Changes in the Male Mouse Olfactory Bulb and Their Correlation with Olfactory-Driven Behavior

Bontempi, Pietro / Ricatti, Maria Jimena / Sandri, Marco / Nicolato, Elena / Mucignat-Caretta, Carla / Zancanaro, Carlo

Biology (Basel). 2023 Feb. 28, v. 12, no. 3

2023

Abstract: Olfactory areas in mammalian brains are linked to centers that modulate behavior. During aging, sensitivity to odors decreases and structural changes are described in olfactory areas. We explored, in two groups of male mice (young and elderly, 6 and 19 ... ...

Abstract	Olfactory areas in mammalian brains are linked to centers that modulate behavior. During aging, sensitivity to odors decreases and structural changes are described in olfactory areas. We explored, in two groups of male mice (young and elderly, 6 and 19 months old, respectively), the link between the changes in olfactory bulb structure, detected with magnetic resonance imaging, and behavioral changes in a battery of tests on motor, olfactory, cognitive performance, and emotional reactivity. The behavioral pattern of elderly mice appears less anxious, being less scared by new situations. Additionally, the olfactory bulb of young and elderly mice differed in two variables derived from magnetic resonance imaging (fractional anisotropy and T2 maps). A random forest approach allowed to select the variables most predictive of the differences between young and elderly mice, and correlations were found between three behavioral variables indicative of anxious behavior and the two magnetic resonance variables mentioned above. These data suggest that in the living mouse, it is possible to describe co-occurring age-related behavioral and structural changes in the olfactory bulb. These data serve as a basis for studies on normal and pathological aging in the mouse, but also open new opportunities for in vivo human aging studies.
Keywords	anisotropy ; cognition ; elderly ; humans ; magnetism ; males ; mice ; olfactory bulb
Language	English
Dates of publication	2023-0228
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12030381
Database	NAL-Catalogue (AGRICOLA)

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