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Article ; Online: Extracellular Vesicles and Exosomes in the Control of the Musculoskeletal Health.

Penna, Fabio / Garcia-Castillo, Lorena / Costelli, Paola

2024 Volume 22, Issue 2, Page(s) 257–265

Abstract: Purpose of review: The present review will highlight recent reports supporting the relevance of extracellular vesicles to the musculoskeletal system in health and disease.: Recent findings: Preserving the health of the musculoskeletal system is ... ...

Abstract	Purpose of review: The present review will highlight recent reports supporting the relevance of extracellular vesicles to the musculoskeletal system in health and disease. Recent findings: Preserving the health of the musculoskeletal system is important to maintain a good quality of life, and the bone-muscle crosstalk is crucial in this regard. This latter is largely mediated by extracellular vesicles released by the different cell populations residing in muscle and bone, which deliver cargoes, microRNAs, and proteins being the most relevant ones, to target cells. Extracellular vesicles could be exploited as therapeutic tools, in view of their resistance to destruction in the biological fluid and of the possibility to be functionalized according to the need. Extracellular vesicles are recognized as crucial players in the bone-muscle cross-talk. Additional studies however are required to refine their use as biomarkers of early alterations of the musculoskeletal system, and as potential therapeutic tools.
MeSH term(s)	Humans ; Extracellular Vesicles/metabolism ; Exosomes/metabolism ; MicroRNAs ; Muscle, Skeletal/metabolism ; Musculoskeletal Diseases/metabolism ; Bone and Bones/metabolism ; Biomarkers/metabolism ; Musculoskeletal System/metabolism
Chemical Substances	MicroRNAs ; Biomarkers
Language	English
Publishing date	2024-03-01
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-024-00866-2
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Article ; Online: Targeting Epigenetic Regulators with HDAC and BET Inhibitors to Modulate Muscle Wasting.

Nevi, Lorenzo / Pöllänen, Noora / Penna, Fabio / Caretti, Giuseppina

International journal of molecular sciences

2023 Volume 24, Issue 22

Abstract: Epigenetic changes contribute to the profound alteration in the transcriptional program associated with the onset and progression of muscle wasting in several pathological conditions. Although HDACs and their inhibitors have been extensively studied in ... ...

Abstract	Epigenetic changes contribute to the profound alteration in the transcriptional program associated with the onset and progression of muscle wasting in several pathological conditions. Although HDACs and their inhibitors have been extensively studied in the field of muscular dystrophies, the potential of epigenetic inhibitors has only been marginally explored in other disorders associated with muscle atrophy, such as in cancer cachexia and sarcopenia. BET inhibitors represent a novel class of recently developed epigenetic drugs that display beneficial effects in a variety of diseases beyond malignancies. Based on the preliminary in vitro and preclinical data, HDACs and BET proteins contribute to the pathogenesis of cancer cachexia and sarcopenia, modulating processes related to skeletal muscle mass maintenance and/or metabolism. Thus, epigenetic drugs targeting HDACs and BET proteins may emerge as promising strategies to reverse the catabolic phenotype associated with cachexia and sarcopenia. Further preclinical studies are warranted to delve deeper into the molecular mechanisms associated with the functions of HDACs and BET proteins in muscle atrophy and to establish whether their epigenetic inhibitors represent a prospective therapeutic avenue to alleviate muscle wasting.
MeSH term(s)	Humans ; Antineoplastic Agents/pharmacology ; Cachexia/metabolism ; Epigenesis, Genetic ; Muscle, Skeletal/metabolism ; Muscular Atrophy/drug therapy ; Muscular Atrophy/genetics ; Neoplasms/metabolism ; Proteins/metabolism ; Sarcopenia/metabolism ; Histone Deacetylases/metabolism
Chemical Substances	Antineoplastic Agents ; Proteins ; DNER protein, human ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2023-11-16
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/ijms242216404
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Article: Amino Acids in Cancer and Cachexia: An Integrated View.

Ragni, Maurizio / Fornelli, Claudia / Nisoli, Enzo / Penna, Fabio

Cancers

2022 Volume 14, Issue 22

Abstract: Rapid tumor growth requires elevated biosynthetic activity, supported by metabolic rewiring occurring both intrinsically in cancer cells and extrinsically in the cancer host. The Warburg effect is one such example, burning glucose to produce a continuous ...

Abstract	Rapid tumor growth requires elevated biosynthetic activity, supported by metabolic rewiring occurring both intrinsically in cancer cells and extrinsically in the cancer host. The Warburg effect is one such example, burning glucose to produce a continuous flux of biomass substrates in cancer cells at the cost of energy wasting metabolic cycles in the host to maintain stable glycemia. Amino acid (AA) metabolism is profoundly altered in cancer cells, which use AAs for energy production and for supporting cell proliferation. The peculiarities in cancer AA metabolism allow the identification of specific vulnerabilities as targets of anti-cancer treatments. In the current review, specific approaches targeting AAs in terms of either deprivation or supplementation are discussed. Although based on opposed strategies, both show, in vitro and in vivo, positive effects. Any AA-targeted intervention will inevitably impact the cancer host, who frequently already has cachexia. Cancer cachexia is a wasting syndrome, also due to malnutrition, that compromises the effectiveness of anti-cancer drugs and eventually causes the patient's death. AA deprivation may exacerbate malnutrition and cachexia, while AA supplementation may improve the nutritional status, counteract cachexia, and predispose the patient to a more effective anti-cancer treatment. Here is provided an attempt to describe the AA-based therapeutic approaches that integrate currently distant points of view on cancer-centered and host-centered research, providing a glimpse of several potential investigations that approach cachexia as a unique cancer disease.
Language	English
Publishing date	2022-11-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14225691
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Article ; Online: Exercise and Exercise Mimetics for the Treatment of Musculoskeletal Disorders.

Cento, Alessia S / Leigheb, Massimiliano / Caretti, Giuseppina / Penna, Fabio

Current osteoporosis reports

2022 Volume 20, Issue 5, Page(s) 249–259

Abstract: Purpose of review: The incidence of musculoskeletal disorders affecting bones, joints, and muscles is dramatically increasing in parallel with the increased longevity of the worldwide population, severely impacting on the individual's quality of life ... ...

Abstract	Purpose of review: The incidence of musculoskeletal disorders affecting bones, joints, and muscles is dramatically increasing in parallel with the increased longevity of the worldwide population, severely impacting on the individual's quality of life and on the healthcare costs. Inactivity and sedentary lifestyle are nowadays considered the main drivers of age-associated musculoskeletal disorders and exercise may counteract such alterations also in other bone- and muscle-centered disorders. This review aims at clarifying the potential use of exercise training to improve musculoskeletal health. Recent findings: Both the skeletal muscle and the bone are involved in a complex crosstalk determining, in part through tissue-specific and inflammatory/immune released factors, the occurrence of musculoskeletal disorders. Exercise is able to modulate the levels of those molecules and several associated molecular pathways. Evidence from preclinical and clinical trials supports the adoption of exercise and the future use of exercise mimicking drugs will optimize the care of individuals with musculoskeletal disorders.
MeSH term(s)	Exercise/physiology ; Exercise Therapy ; Humans ; Musculoskeletal Diseases/therapy ; Quality of Life ; Sedentary Behavior
Language	English
Publishing date	2022-07-26
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-022-00739-6
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Article ; Online: The BET inhibitor JQ1 targets fat metabolism and counteracts obesity.

Fornelli, Claudia / Sofia Cento, Alessia / Nevi, Lorenzo / Mastrocola, Raffaella / Ferreira Alves, Gustavo / Caretti, Giuseppina / Collino, Massimo / Penna, Fabio

Journal of advanced research

2024

Abstract: Introduction: Obesity, one of the most frequent health problems in the adult population, is a condition characterized by excessive white adipose tissue accumulation and accompanied by the increased risk to develop other disorders such as type II ... ...

Abstract	Introduction: Obesity, one of the most frequent health problems in the adult population, is a condition characterized by excessive white adipose tissue accumulation and accompanied by the increased risk to develop other disorders such as type II diabetes, cardiovascular disorders, physical disability, frailty and sarcopenia. Total fat mass frequently increases during aging, often coexisting with sarcopenia, thus resulting in an emerging condition defined sarcopenic obesity (SO). Our previous data demonstrated the relevant role of the bromo and extra-terminal domain (BET) proteins inhibitor JQ1 in attenuating inflammation and fibrosis in sarcopenic mice. Moreover, we preliminarily observed that JQ1 administration markedly reduces white adipose tissue mass, suggesting a potential role of BET proteins on visceral fat deposition during aging. Objectives: Starting from those observations, the aim of this study was to investigate the ability of JQ1 to reduce adiposity in a chronic diet-induced obesity (DIO) mouse model mimicking the human metabolic syndrome. Methods: Male C57BL/6J mice were divided in subgroups, either fed a standard diet or a high fat diet for 22 or 12 weeks, treated over the last 14 days with JQ1 or with vehicle. Results: The results showed that JQ1 administration reduces fat mass, preserving skeletal muscle mass and function. A direct JQ1 lipolytic effect was demonstrated on mature adipocyte cultures. JQ1-mediated loss of adipose tissue mass was not associated with systemic inflammation or with lipid accumulation in muscle and liver. JQ1 administration did not impinge on skeletal muscle metabolism and oxidative capability, as shown by the lack of significant impact on mitochondrial mass and biogenesis. Conclusion: In conclusion, the current data highlight a potential benefit of JQ1 administration to counteract obesity, suggesting epigenetic modulation as a prospective target in the treatment of obesity and sarcopenic obesity, despite the underlying multiorgan molecular mechanism is still not completely elucidated.
Language	English
Publishing date	2024-02-15
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2541849-X
ISSN	2090-1224 ; 2090-1224
ISSN (online)	2090-1224
ISSN	2090-1224
DOI	10.1016/j.jare.2024.02.001
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Article ; Online: New developments in investigational HDAC inhibitors for the potential multimodal treatment of cachexia.

Penna, Fabio / Costelli, Paola

Expert opinion on investigational drugs

2018 Volume 28, Issue 2, Page(s) 179–189

Abstract: Introduction: Cachexia is a frequent feature of chronic diseases. This syndrome includes loss of body weight, depletion of skeletal muscle mass and altered metabolic homeostasis. Acceleration of protein and energy metabolism, impaired myogenesis, and ... ...

Abstract	Introduction: Cachexia is a frequent feature of chronic diseases. This syndrome includes loss of body weight, depletion of skeletal muscle mass and altered metabolic homeostasis. Acceleration of protein and energy metabolism, impaired myogenesis, and systemic inflammation contribute to cachexia. Its occurrence impinges on treatment tolerance and on the quality of life of the patient, however, no effective therapy is available yet. Areas covered: This review focuses on the use of histone deacetylase inhibitors as pharmacological tools to prevent or delay cachexia, with reference to muscle wasting. Expert opinion: Novel histone deacetylase inhibitors could be considered as exercise mimetics and this supports their use as a treatment for muscle-wasting associated diseases, such as cachexia. The ability of some of these inhibitors to modulate the release of extracellular vesicles from tumor cells is a potential tool for restricting the development of cancer-induced muscle protein depletion. There are few clinical trials that are testing histone deacetylase inhibitors as a treatment for cachexia; this reflects the lack of robust experimental evidence of effectiveness. The determination of the pathogenic mechanisms of muscle wasting and the identification of suitable histone deacetylase inhibitors that target such mechanisms are necessary.
MeSH term(s)	Animals ; Cachexia/drug therapy ; Cachexia/etiology ; Cachexia/physiopathology ; Combined Modality Therapy ; Drug Development ; Drugs, Investigational/pharmacology ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Neoplasms/complications ; Quality of Life
Chemical Substances	Drugs, Investigational ; Histone Deacetylase Inhibitors
Language	English
Publishing date	2018-12-14
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1182884-5
ISSN	1744-7658 ; 0967-8298 ; 1354-3784
ISSN (online)	1744-7658
ISSN	0967-8298 ; 1354-3784
DOI	10.1080/13543784.2019.1557634
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Article ; Online: The Redox Balance: A Target for Interventions Against Muscle Wasting in Cancer Cachexia?

Penna, Fabio / Ballarò, Riccardo / Costelli, Paola

Antioxidants & redox signaling

2020 Volume 33, Issue 8, Page(s) 542–558

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Animals ; Biomarkers ; Cachexia/etiology ; Energy Metabolism/drug effects ; Exercise ; Homeostasis ; Humans ; Mitochondria, Muscle/drug effects ; Mitochondria, Muscle/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Neoplasms/complications ; Neoplasms/metabolism ; Oxidation-Reduction/drug effects ; Oxidative Stress
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2020.8041
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Article ; Online: Mitochondrial Dysfunction in Cancer Cachexia: Impact on Muscle Health and Regeneration.

Beltrà, Marc / Pin, Fabrizio / Ballarò, Riccardo / Costelli, Paola / Penna, Fabio

Cells

2021 Volume 10, Issue 11

Abstract: Cancer cachexia is a frequently neglected debilitating syndrome that, beyond representing a primary cause of death and cancer therapy failure, negatively impacts on patients' quality of life. Given the complexity of its multisystemic pathogenesis, ... ...

Abstract	Cancer cachexia is a frequently neglected debilitating syndrome that, beyond representing a primary cause of death and cancer therapy failure, negatively impacts on patients' quality of life. Given the complexity of its multisystemic pathogenesis, affecting several organs beyond the skeletal muscle, defining an effective therapeutic approach has failed so far. Revamped attention of the scientific community working on cancer cachexia has focused on mitochondrial alterations occurring in the skeletal muscle as potential triggers of the complex metabolic derangements, eventually leading to hypercatabolism and tissue wasting. Mitochondrial dysfunction may be simplistically viewed as a cause of energy failure, thus inducing protein catabolism as a compensatory mechanism; however, other peculiar cachexia features may depend on mitochondria. On the one side, chemotherapy also impacts on muscle mitochondrial function while, on the other side, muscle-impaired regeneration may result from insufficient energy production from damaged mitochondria. Boosting mitochondrial function could thus improve the energetic status and chemotherapy tolerance, and relieve the myogenic process in cancer cachexia. In the present work, a focused review of the available literature on mitochondrial dysfunction in cancer cachexia is presented along with preliminary data dissecting the potential role of stimulating mitochondrial biogenesis via PGC-1α overexpression in distinct aspects of cancer-induced muscle wasting.
MeSH term(s)	Animals ; Cachexia/complications ; Cachexia/pathology ; Humans ; Mitochondria/pathology ; Muscle Development ; Muscles/physiopathology ; Neoplasms/complications ; Neoplasms/pathology ; Regeneration
Language	English
Publishing date	2021-11-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10113150
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Article ; Online: Targeting the Activin Receptor Signaling to Counteract the Multi-Systemic Complications of Cancer and Its Treatments.

Hulmi, Juha J / Nissinen, Tuuli A / Penna, Fabio / Bonetto, Andrea

Cells

2021 Volume 10, Issue 3

Abstract: Muscle wasting, i.e., cachexia, frequently occurs in cancer and associates with poor prognosis and increased morbidity and mortality. Anticancer treatments have also been shown to contribute to sustainment or exacerbation of cachexia, thus affecting ... ...

Abstract	Muscle wasting, i.e., cachexia, frequently occurs in cancer and associates with poor prognosis and increased morbidity and mortality. Anticancer treatments have also been shown to contribute to sustainment or exacerbation of cachexia, thus affecting quality of life and overall survival in cancer patients. Pre-clinical studies have shown that blocking activin receptor type 2 (ACVR2) or its ligands and their downstream signaling can preserve muscle mass in rodents bearing experimental cancers, as well as in chemotherapy-treated animals. In tumor-bearing mice, the prevention of skeletal and respiratory muscle wasting was also associated with improved survival. However, the definitive proof that improved survival directly results from muscle preservation following blockade of ACVR2 signaling is still lacking, especially considering that concurrent beneficial effects in organs other than skeletal muscle have also been described in the presence of cancer or following chemotherapy treatments paired with counteraction of ACVR2 signaling. Hence, here, we aim to provide an up-to-date literature review on the multifaceted anti-cachectic effects of ACVR2 blockade in preclinical models of cancer, as well as in combination with anticancer treatments.
MeSH term(s)	Activin Receptors, Type II/metabolism ; Cachexia/etiology ; Cachexia/physiopathology ; Humans ; Neoplasms/complications ; Neoplasms/mortality ; Signal Transduction ; Survival Analysis
Chemical Substances	Activin Receptors, Type II (EC 2.7.11.30)
Language	English
Publishing date	2021-02-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10030516
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Article ; Online: Targeting Mitochondria and Oxidative Stress in Cancer- and Chemotherapy-Induced Muscle Wasting.

Huot, Joshua R / Baumfalk, Dryden / Resendiz, Aridai / Bonetto, Andrea / Smuder, Ashley J / Penna, Fabio

Antioxidants & redox signaling

2022 Volume 38, Issue 4-6, Page(s) 352–370

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Humans ; Cachexia/etiology ; Muscle, Skeletal/metabolism ; Neoplasms/metabolism ; Muscular Atrophy/chemically induced ; Mitochondria/metabolism ; Oxidative Stress ; Antineoplastic Agents/adverse effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2022-12-29
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2022.0149
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