Alfredo Gimenez-Cassina Group
Our current research focuses on understanding how signaling cascades regulate energy metabolism, with a special focus on mitochondria. Mitochondrial metabolism plays a key role in cellular physiology, which is underscored by the fact that mitochondrial dysfunction and metabolic decline have been linked to several pathologies, such as diabetes or neurological disorders. Our previous studies have shown that manipulation of the metabolic program constitutes a promising therapeutic strategy to treat disorders in which metabolic dysfunction is a central feature. Therefore understanding the molecular mechanisms that modulate energy metabolism and mitochondrial function will contribute to gain insight into the underpinnings responsible for the pathogenesis of such diseases.
In particular, we are interested in:
- Understanding how nutrients are sensed and utilized, and how select utilization of different carbon substrates impact cellular viability and physiology.
- Identification and characterization of signaling mechanisms that modulate energy metabolism.
- Evaluation of therapeutic strategies based on modulating mitochondrial metabolism
To address these questions we use a multidisciplinary approach that combines cellular biology, metabolic flux analysis, biochemistry, proteomics, molecular biology and in vivo studies. Our ultimate goal is to identify integrative mechanisms of regulation of energy metabolism and to develop novel therapeutic strategies for disorders in which aberrations in metabolism play a prominent role.
|Alfredo Gimenez-Cassina||Senior researcher|
Food for thought: Impact of metabolism on neuronal excitability.
Exp. Cell Res. 2017 11;360(1):41-46
Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness.
Sci Rep 2016 06;6():28080
Regulation of mitochondrial nutrient and energy metabolism by BCL-2 family proteins.
Trends Endocrinol. Metab. 2015 Apr;26(4):165-75
Regulation of hepatic energy metabolism and gluconeogenesis by BAD.
Cell Metab. 2014 Feb;19(2):272-84
Chronic inhibition of glycogen synthase kinase-3 protects against rotenone-induced cell death in human neuron-like cells by increasing BDNF secretion.
Neurosci. Lett. 2012 Dec;531(2):182-7
BAD-dependent regulation of fuel metabolism and K(ATP) channel activity confers resistance to epileptic seizures.
Neuron 2012 May;74(4):719-30
Mitochondrial hexokinase II promotes neuronal survival and acts downstream of glycogen synthase kinase-3.
J. Biol. Chem. 2009 Jan;284(5):3001-11
|Camilla Faoro||R&D Student|
|Rodrigo García-Martín||R&D Student|
|Anna Vidina||Summer BSc Student|
|Ana Canerina Luis Amaro||Visiting PhD student (Universidad de La Laguna, Tenerife, Spain)|
|Mauro Agrò||Visiting PhD Student (Universidad Autónoma de Madrid, Spain, supported by a short-term EMBO Fellowship)|
|Nerea Gómez de San José||Visiting BSc Student (Universidad Autónoma de Madrid, Spain, supported by the ERASMUS Program)|