Prof. Dr. Ciro Isidoro
Department of Health Sciences, Università del Piemonte Orientale, Novara, Piedmont, Italy
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Academic Career Length
41Years (1986-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications12 February 2008 in Proceedings of the National Academy of Sciences
Journal Article
Francesco Fornai
Patrizia LongoneLCLuisa Cafaro
Luisa Cafaro
OKOlga Kastsiuchenka
Olga Kastsiuchenka
Michela FerrucciAPAntonio Paparelli
Antonio Paparelli
+10
ALS is a devastating neurodegenerative disorder with no effective treatment. In the present study, we found that daily doses of lithium, leading to plasma levels ranging from 0.4 to 0.8 mEq/liter, delay disease progression in human patients affected by ALS. None of the patients treated with lithium died during the 15 months of the follow-up, and disease progression was markedly attenuated when compared with age-, disease duration-, and sex-matched control patients treated with riluzole for the same amount of time. In a parallel study on a genetic ALS animal model, the G93A mouse, we found a marked neuroprotection by lithium, which delayed disease onset and duration and augmented the life span. These effects were concomitant with activation of autophagy and an increase in the number of the mitochondria in motor neurons and suppressed reactive astrogliosis. Again, lithium reduced the slow necrosis characterized by mitochondrial vacuolization and increased the number of neurons counted in lamina VII that were severely affected in saline-treated G93A mice. After lithium administration in G93A mice, the number of these neurons was higher even when compared with saline-treated WT. All these mechanisms may contribute to the effects of lithium, and these results offer a promising perspective for the treatment of human patients affected by ALS.
19 March 2008 in European Journal of Neuroscience
Journal Article
THTadanori Hamano
Tadanori Hamano
TGTania F. Gendron
Tania F. Gendron
ECEna Causevic
Ena Causevic
SYShu‐Hui Yen
Shu‐Hui Yen
WLWen‐Lang Lin
Wen‐Lang Lin
LKLi‐Wen Ko
Li‐Wen Ko
+2
26 April 2016 in Medicinal Research Reviews
Journal Article
CVChiara Vidoni
Chiara Vidoni
CFCarlo Follo
Carlo FolloMSMiriam Savino
Miriam Savino
Mariarosa Anna Beatrice MeloneCiro Isidoro17 August 2012 in Molecular Neurobiology
Journal Article
Elzbieta JandaCiro IsidoroCCCristina Carresi
Cristina CarresiVMVincenzo Mollace
Vincenzo Mollace
1 March 2015 in EBioMedicine
Journal Article
HTHao Tang
Hao Tang
SSSalwa Sebti
Salwa Sebti
RTRossella Titone
Rossella TitoneYZYunyun Zhou
Yunyun Zhou
Ciro IsidoroBLBeth Levine
Beth Levine +5
Both BRCA1 and Beclin 1 (BECN1) are tumor suppressor genes, which are in close proximity on the human chromosome 17q21 breast cancer tumor susceptibility locus and are often concurrently deleted. However, their importance in sporadic human breast cancer is not known. To interrogate the effects of BECN1 and BRCA1 in breast cancer, we studied their mRNA expression patterns in breast cancer patients from two large datasets: The Cancer Genome Atlas (TCGA) (n = 1067) and the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) (n = 1992). In both datasets, low expression of BECN1 was more common in HER2-enriched and basal-like (mostly triple-negative) breast cancers compared to luminal A/B intrinsic tumor subtypes, and was also strongly associated with TP53 mutations and advanced tumor grade. In contrast, there was no significant association between low BRCA1 expression and HER2-enriched or basal-like subtypes, TP53 mutations or tumor grade. In addition, low expression of BECN1 (but not low BRCA1) was associated with poor prognosis, and BECN1 (but not BRCA1) expression was an independent predictor of survival. These findings suggest that decreased mRNA expression of the autophagy gene BECN1 may contribute to the pathogenesis and progression of HER2-enriched, basal-like, and TP53 mutant breast cancers.
31 March 2016 in Cell Death & Disease
Journal Article
PFPaola Fortini
Paola FortiniCFC Ferretti
C Ferretti
Egidio IorioMCM Cagnin
M Cagnin
LGL Garribba
L Garribba
EDEugenia Dogliotti
Eugenia Dogliotti +8
Although the mechanisms controlling skeletal muscle homeostasis have been identified, there is a lack of knowledge of the integrated dynamic processes occurring during myogenesis and their regulation. Here, metabolism, autophagy and differentiation were concomitantly analyzed in mouse muscle satellite cell (MSC)-derived myoblasts and their cross-talk addressed by drug and genetic manipulation. We show that increased mitochondrial biogenesis and activation of mammalian target of rapamycin complex 1 inactivation-independent basal autophagy characterize the conversion of myoblasts into myotubes. Notably, inhibition of autophagic flux halts cell fusion in the latest stages of differentiation and, conversely, when the fusion step of myocytes is impaired the biogenesis of autophagosomes is also impaired. By using myoblasts derived from p53 null mice, we show that in the absence of p53 glycolysis prevails and mitochondrial biogenesis is strongly impaired. P53 null myoblasts show defective terminal differentiation and attenuated basal autophagy when switched into differentiating culture conditions. In conclusion, we demonstrate that basal autophagy contributes to a correct execution of myogenesis and that physiological p53 activity is required for muscle homeostasis by regulating metabolism and by affecting autophagy and differentiation.
About Me
Ciro Isidoro is a full Professor of
General Pathology at the Department of Health Sciences, University of Piemonte
Orientale (Novara, Italy). He holds a Doctor of Science degree in Biological
Sciences (Magna Cum Laude) and a Doctor of Medicine and Surgery degree (Magna
Cum Laude). He has been a PhD fellow and Assistant Researcher at the
Institut für Pathobiochemie, Westfälische Wilhelms-Universität Münster in
Germany. Professor Isidoro has been awarded Professor Honoris Causa by the
Faculty of Medicine and Pharmacy at the Université de la Franche-Comté in
Besançon, France. He is a visiting professor at the Siriraj Faculty of
Medicine, Mahidol University in Bangkok, Thailand, and at the Department of
Cell Biology, Oklahoma University Health Science Center in Oklahoma City, USA.
Professor Isidoro is the Editor-in-Chief of the Journal of Traditional and
Complementary Medicine and of the Journal of Cancer and Metastasis Treatment,
and Associate Editor of Autophagy, Molecular Carcinogenesis, Cancers,
Frontiers in Oncology, Cells, Biomedicines, and the International Journal of Molecular
Sciences, among others. Professor Isidoro is a globally recognized expert in
autophagy and lysosome biogenesis. His research primarily focuses on the role
of autophagy-lysosomal degradation in cancer, neurodegenerative diseases, and
the epigenetic mechanisms of anti-tumor nutraceuticals. Professor Isidoro
has been listed as a TOP 2% scientist in the world in 2023 and a TOP Italian
scientist.