TY - JOUR
T1 - Growing role of S100B protein as a putative therapeutic target for neurological -and nonneurological- disorders
AU - Michetti, Fabrizio
AU - Di Sante, Gabriele
AU - Clementi, Maria Elisabetta
AU - Sampaolese, Beatrice
AU - Casalbore, Patrizia
AU - Volonté, Cinzia
AU - Romano Spica, Vincenzo
AU - Parnigotto, Pier Paolo
AU - Di Liddo, Rosa
AU - Amadio, Susanna
AU - Ria, Francesco
PY - 2021
Y1 - 2021
N2 - S100B is a calcium-binding protein mainly expressed by astrocytes, but also localized in other definite neural and extra-neural cell types. While its presence in biological fluids is widely recognized as a reliable biomarker of active injury, growing evidence now indicates that high levels of S100B are suggestive of pathogenic processes in different neural, but also extra-neural, disorders. Indeed, modulation of S100B levels correlates with the occurrence of clinical and/or toxic parameters in experimental models of diseases such as Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, muscular dystrophy, multiple sclerosis, acute neural injury, inflammatory bowel disease, uveal and retinal disorders, obesity, diabetes and cancer, thus directly linking the levels of S100B to pathogenic mechanisms. In general, deletion/inactivation of the protein causes the improvement of the disease, whereas its over-expression/administration induces a worse clinical presentation. This scenario reasonably proposes S100B as a common therapeutic target for several different disorders, also offering new clues to individuate possible unexpected connections among these diseases.
AB - S100B is a calcium-binding protein mainly expressed by astrocytes, but also localized in other definite neural and extra-neural cell types. While its presence in biological fluids is widely recognized as a reliable biomarker of active injury, growing evidence now indicates that high levels of S100B are suggestive of pathogenic processes in different neural, but also extra-neural, disorders. Indeed, modulation of S100B levels correlates with the occurrence of clinical and/or toxic parameters in experimental models of diseases such as Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, muscular dystrophy, multiple sclerosis, acute neural injury, inflammatory bowel disease, uveal and retinal disorders, obesity, diabetes and cancer, thus directly linking the levels of S100B to pathogenic mechanisms. In general, deletion/inactivation of the protein causes the improvement of the disease, whereas its over-expression/administration induces a worse clinical presentation. This scenario reasonably proposes S100B as a common therapeutic target for several different disorders, also offering new clues to individuate possible unexpected connections among these diseases.
KW - S100B, therapeutic target, DAMP
KW - S100B, therapeutic target, DAMP
UR - http://hdl.handle.net/10807/178710
U2 - 10.1016/j.neubiorev.2021.04.035
DO - 10.1016/j.neubiorev.2021.04.035
M3 - Article
SN - 0149-7634
VL - 127
SP - 446
EP - 458
JO - Neuroscience and Biobehavioral Reviews
JF - Neuroscience and Biobehavioral Reviews
ER -