LIVIVO - Search results -

Search results

Result 1 - 10 of total 93

Search options

Article ; Online: Introduction to the Special Issue "Skeletal Muscle Atrophy: Mechanisms at a Cellular Level".

Zuccaro, Emanuela / Marchioretti, Caterina / Pirazzini, Marco / Pennuto, Maria

2023 Volume 12, Issue 3

Abstract: Skeletal muscle is the most abundant tissue in the body and requires high levels of energy to function properly. Skeletal muscle allows voluntary movement and body posture, which require different types of fiber, innervation, energy, and metabolism. Here, ...

Abstract	Skeletal muscle is the most abundant tissue in the body and requires high levels of energy to function properly. Skeletal muscle allows voluntary movement and body posture, which require different types of fiber, innervation, energy, and metabolism. Here, we summarize the contribution received at the time of publication of this Introductory Issue for the Special Issue dedicated to "
MeSH term(s)	Humans ; Muscular Atrophy/pathology ; Muscle, Skeletal/metabolism
Language	English
Publishing date	2023-02-03
Publishing country	Switzerland
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12030502
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Editorial Comment to Castration-resistant prostate cancer diagnosed during leuprorelin treatment for spinal and bulbar muscular atrophy.

Pennuto, Maria / Montopoli, Monica / Rinaldi, Carlo

IJU case reports

2022 Volume 5, Issue 4, Page(s) 254

Language	English
Publishing date	2022-05-10
Publishing country	Australia
Document type	Editorial
ISSN	2577-171X
ISSN (online)	2577-171X
DOI	10.1002/iju5.12465
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Introduction to the Special Issue “Skeletal Muscle Atrophy

Emanuela Zuccaro / Caterina Marchioretti / Marco Pirazzini / Maria Pennuto

Cells, Vol 12, Iss 502, p

Mechanisms at a Cellular Level”

2023 Volume 502

Abstract	Skeletal muscle is the most abundant tissue in the body and requires high levels of energy to function properly. Skeletal muscle allows voluntary movement and body posture, which require different types of fiber, innervation, energy, and metabolism. Here, we summarize the contribution received at the time of publication of this Introductory Issue for the Special Issue dedicated to “ Skeletal Muscle Atrophy: Mechanisms at a Cellular Level ”. The Special Issue is divided into three sections. The first is dedicated to skeletal muscle pathophysiology, the second to disease mechanisms, and the third to therapeutic development.
Keywords	muscle atrophy ; muscle proteostasis and disuse ; atrogenes ; sarcopenia ; neuromuscular disorder ; myopathies ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Spinal and bulbar muscular atrophy: From molecular pathogenesis to pharmacological intervention targeting skeletal muscle.

Marchioretti, Caterina / Andreotti, Roberta / Zuccaro, Emanuela / Lieberman, Andrew P / Basso, Manuela / Pennuto, Maria

Current opinion in pharmacology

2023 Volume 71, Page(s) 102394

Abstract: The clinical characteristics of SBMA, also known as Kennedy's disease (OMIM 313200), were initially documented by Dr. H Kawahara in the 18th century and a hundred years later by Dr. W. Kennedy. SBMA is a neuromuscular disease caused by expansions of a ... ...

Abstract	The clinical characteristics of SBMA, also known as Kennedy's disease (OMIM 313200), were initially documented by Dr. H Kawahara in the 18th century and a hundred years later by Dr. W. Kennedy. SBMA is a neuromuscular disease caused by expansions of a CAG microsatellite tandem repeat in exon 1 of the androgen receptor (AR) gene located on the X chromosome. These expansions result in the production of AR with an aberrantly expanded polyglutamine (polyQ) tract. In this review, we explore recent advancements in the significance of gene expression changes in skeletal muscle and discuss how pharmacological interventions targeting this aspect of disease pathogenesis can potentially be translated into therapies for SBMA patients.
MeSH term(s)	Humans ; Bulbo-Spinal Atrophy, X-Linked/drug therapy ; Bulbo-Spinal Atrophy, X-Linked/genetics ; Bulbo-Spinal Atrophy, X-Linked/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Receptors, Androgen/therapeutic use ; Muscle, Skeletal/metabolism ; Muscular Atrophy
Chemical Substances	Receptors, Androgen
Language	English
Publishing date	2023-07-16
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2023.102394
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5608: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Motor Neuron Diseases and Neuroprotective Peptides: A Closer Look to Neurons.

Zuccaro, Emanuela / Piol, Diana / Basso, Manuela / Pennuto, Maria

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 723871

Abstract: Motor neurons (MNs) are specialized neurons responsible for muscle contraction that specifically degenerate in motor neuron diseases (MNDs), such as amyotrophic lateral sclerosis (ALS), spinal and bulbar muscular atrophy (SBMA), and spinal muscular ... ...

Abstract	Motor neurons (MNs) are specialized neurons responsible for muscle contraction that specifically degenerate in motor neuron diseases (MNDs), such as amyotrophic lateral sclerosis (ALS), spinal and bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Distinct classes of MNs degenerate at different rates in disease, with a particular class named fast-fatigable MNs (FF-MNs) degenerating first. The etiology behind the selective vulnerability of FF-MNs is still largely under investigation. Among the different strategies to target MNs, the administration of protective neuropeptides is one of the potential therapeutic interventions. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide with beneficial effects in many neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and more recently SBMA. Another neuropeptide that has a neurotrophic effect on MNs is insulin-like growth factor 1 (IGF-1), also known as somatomedin C. These two peptides are implicated in the activation of neuroprotective pathways exploitable in the amelioration of pathological outcomes related to MNDs.
Language	English
Publishing date	2021-09-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.723871
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Pituitary Adenylyl Cyclase Activating Polypeptide (PACAP) Signaling and the Cell Cycle Machinery in Neurodegenerative Diseases.

Polanco, María José / Pennuto, Maria

Current pharmaceutical design

2018 Volume 24, Issue 33, Page(s) 3878–3891

Abstract: Pituitary adenylyl cyclase activating polypeptide (PACAP) is a neuropeptide with great neuroprotective effects and remarkable therapeutic potential. PACAP activates several cellular pathways to exert its protective effects. Emerging evidence shows that ... ...

Abstract	Pituitary adenylyl cyclase activating polypeptide (PACAP) is a neuropeptide with great neuroprotective effects and remarkable therapeutic potential. PACAP activates several cellular pathways to exert its protective effects. Emerging evidence shows that PACAP can modify the levels and activity of cell cycle components involved in neurodegeneration to protect neurons from death. Cell cycle is a highly regulated process that controls the balance between proliferation, differentiation and death of every cell in the body. Aberrant expression and function of components of the cell cycle machinery have been linked to neurodegenerative diseases, in which different types of neuronal cells become dysfunctional and die in response to toxic insults. Since neurons are postmitotic cells, re-entry into the cell cycle has been shown to be pathological and contributes to the process of neurodegeneration. Moreover, an increasing number of studies highlight the importance of the role of cell cycle components outside the cell cycle and their involvement in neurodegenerative disorders. Here, we discuss the pleiotropic effects of PACAP on cell cycle machinery and the implication for the treatment of neurodegenerative diseases.
MeSH term(s)	Animals ; Cell Cycle/drug effects ; Humans ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/metabolism ; Pituitary Adenylate Cyclase-Activating Polypeptide/metabolism ; Pituitary Adenylate Cyclase-Activating Polypeptide/pharmacology ; Signal Transduction/drug effects
Chemical Substances	Pituitary Adenylate Cyclase-Activating Polypeptide
Language	English
Publishing date	2018-11-26
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612825666181127102311
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4714: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Insulin-like growth factor 1 signaling in motor neuron and polyglutamine diseases: From molecular pathogenesis to therapeutic perspectives.

Pennuto, Maria / Pandey, Udai Bhan / Polanco, María José

Frontiers in neuroendocrinology

2020 Volume 57, Page(s) 100821

Abstract: The pleiotropic peptide insulin-like growth factor 1 (IGF-I) regulates human body homeostasis and cell growth. IGF-I activates two major signaling pathways, namely phosphoinositide-3-kinase (PI3K)/protein kinase B (PKB/Akt) and Ras/extracellular signal- ... ...

Abstract	The pleiotropic peptide insulin-like growth factor 1 (IGF-I) regulates human body homeostasis and cell growth. IGF-I activates two major signaling pathways, namely phosphoinositide-3-kinase (PI3K)/protein kinase B (PKB/Akt) and Ras/extracellular signal-regulated kinase (ERK), which contribute to brain development, metabolism and function as well as to neuronal maintenance and survival. In this review, we discuss the general and tissue-specific effects of the IGF-I pathways. In addition, we present a comprehensive overview examining the role of IGF-I in neurodegenerative diseases, such as spinal and muscular atrophy, amyotrophic lateral sclerosis, and polyglutamine diseases. In each disease, we analyze the disturbances of the IGF-I pathway, the modification of the disease protein by IGF-I signaling, and the therapeutic strategies based on the use of IGF-I developed to date. Lastly, we highlight present and future considerations in the use of IGF-I for the treatment of these disorders.
MeSH term(s)	Amyotrophic Lateral Sclerosis/physiopathology ; Animals ; Glutamine/genetics ; Humans ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/physiology ; MAP Kinase Signaling System/physiology ; Motor Neurons/metabolism ; Muscular Atrophy, Spinal/physiopathology ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/physiopathology ; Peptides ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/physiology ; ras Proteins/metabolism
Chemical Substances	Peptides ; Glutamine (0RH81L854J) ; polyglutamine (26700-71-0) ; Insulin-Like Growth Factor I (67763-96-6) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2020-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	390985-2
ISSN	1095-6808 ; 0532-7466 ; 0091-3022
ISSN (online)	1095-6808
ISSN	0532-7466 ; 0091-3022
DOI	10.1016/j.yfrne.2020.100821
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3423: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 443: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The pVHL neglected functions, a tale of hypoxia-dependent and -independent regulations in cancer.

Minervini, Giovanni / Pennuto, Maria / Tosatto, Silvio C E

Open biology

2020 Volume 10, Issue 7, Page(s) 200109

Abstract: The von Hippel-Lindau protein (pVHL) is a tumour suppressor mainly known for its role as master regulator of hypoxia-inducible factor (HIF) activity. Functional inactivation of pVHL is causative of the von Hippel-Lindau disease, an inherited ... ...

Abstract	The von Hippel-Lindau protein (pVHL) is a tumour suppressor mainly known for its role as master regulator of hypoxia-inducible factor (HIF) activity. Functional inactivation of pVHL is causative of the von Hippel-Lindau disease, an inherited predisposition to develop different cancers. Due to its impact on human health, pVHL has been widely studied in the last few decades. However, investigations mostly focus on its role in degrading HIFs, whereas alternative pVHL protein-protein interactions and functions are insistently surfacing in the literature. In this review, we analyse these almost neglected functions by dissecting specific conditions in which pVHL is proposed to have differential roles in promoting cancer. We reviewed its role in regulating phosphorylation as a number of works suggest pVHL to act as an inhibitor by either degrading or promoting downregulation of specific kinases. Further, we summarize hypoxia-dependent and -independent pVHL interactions with multiple protein partners and discuss their implications in tumorigenesis.
MeSH term(s)	DNA-Binding Proteins/genetics ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Neoplasms/genetics ; Protein Binding/genetics ; Transcription Factors/genetics ; Tumor Hypoxia/genetics ; Tumor Suppressor Proteins/genetics ; Ubiquitin-Protein Ligases ; Von Hippel-Lindau Tumor Suppressor Protein/genetics
Chemical Substances	DNA-Binding Proteins ; Hypoxia-Inducible Factor 1, alpha Subunit ; Transcription Factors ; Tumor Suppressor Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2020-07-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2630944-0
ISSN	2046-2441 ; 2046-2441
ISSN (online)	2046-2441
ISSN	2046-2441
DOI	10.1098/rsob.200109
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Skeletal Muscle Pathogenesis in Polyglutamine Diseases.

Marchioretti, Caterina / Zuccaro, Emanuela / Pandey, Udai Bhan / Rosati, Jessica / Basso, Manuela / Pennuto, Maria

Cells

2022 Volume 11, Issue 13

Abstract: Polyglutamine diseases are characterized by selective dysfunction and degeneration of specific types of neurons in the central nervous system. In addition, nonneuronal cells can also be affected as a consequence of primary degeneration or due to neuronal ...

Abstract	Polyglutamine diseases are characterized by selective dysfunction and degeneration of specific types of neurons in the central nervous system. In addition, nonneuronal cells can also be affected as a consequence of primary degeneration or due to neuronal dysfunction. Skeletal muscle is a primary site of toxicity of polyglutamine-expanded androgen receptor, but it is also affected in other polyglutamine diseases, more likely due to neuronal dysfunction and death. Nonetheless, pathological processes occurring in skeletal muscle atrophy impact the entire body metabolism, thus actively contributing to the inexorable progression towards the late and final stages of disease. Skeletal muscle atrophy is well recapitulated in animal models of polyglutamine disease. In this review, we discuss the impact and relevance of skeletal muscle in patients affected by polyglutamine diseases and we review evidence obtained in animal models and patient-derived cells modeling skeletal muscle.
MeSH term(s)	Animals ; Humans ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy/pathology ; Neurons/metabolism ; Peptides/metabolism
Chemical Substances	Peptides ; polyglutamine (26700-71-0)
Language	English
Publishing date	2022-07-03
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11132105
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Clenbuterol-sensitive delayed outward potassium currents in a cell model of spinal and bulbar muscular atrophy.

Martínez-Rojas, Vladimir A / Arosio, Daniele / Pennuto, Maria / Musio, Carlo

Pflugers Archiv : European journal of physiology

2021 Volume 473, Issue 8, Page(s) 1213–1227

Abstract: Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. SBMA is characterized by selective dysfunction and degeneration of motor neurons in the brainstem and ... ...

Abstract	Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. SBMA is characterized by selective dysfunction and degeneration of motor neurons in the brainstem and spinal cord through still unclear mechanisms in which ion channel modulation might play a central role as for other neurodegenerative diseases. The beta2-adrenergic agonist clenbuterol was observed to ameliorate the SBMA phenotype in mice and patient-derived myotubes. However, the underlying molecular mechanism has yet to be clarified. Here, we unveil that ionic current alterations induced by the expression of polyQ-expanded AR in motor neuron-derived MN-1 cells are attenuated by the administration of clenbuterol. Our combined electrophysiological and pharmacological approach allowed us to reveal that clenbuterol modifies delayed outward potassium currents. Overall, we demonstrated that the protection provided by clenbuterol restores the normal function through the modulation of K
MeSH term(s)	Animals ; Arthropod Proteins ; Bulbo-Spinal Atrophy, X-Linked/etiology ; Bulbo-Spinal Atrophy, X-Linked/metabolism ; Cell Line ; Clenbuterol ; Delayed Rectifier Potassium Channels/metabolism ; Humans ; Mice ; Patch-Clamp Techniques ; Spider Venoms
Chemical Substances	Arthropod Proteins ; Delayed Rectifier Potassium Channels ; GxTX-1E, Plesiophrictus guangxiensis ; Spider Venoms ; Clenbuterol (XTZ6AXU7KN)
Language	English
Publishing date	2021-05-22
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-021-02559-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.35: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito