A5090090006- Muscle Physiology and Disorders
- Exercise and Physiological Responses
- Muscle metabolism and nutrition
- Mesenchymal stem cell research
- Veterinary Equine Medical Research
- Tissue Engineering and Regenerative Medicine
- Genetics, Aging, and Longevity in Model Organisms
- Adipose Tissue and Metabolism
- Autophagy in Disease and Therapy
- Telomeres, Telomerase, and Senescence
- Neurogenetic and Muscular Disorders Research
- Sports Performance and Training
- Mitochondrial Function and Pathology
- Cardiomyopathy and Myosin Studies
- Signaling Pathways in Disease
- Immune cells in cancer
- Nerve injury and regeneration
- Extracellular vesicles in disease
- GDF15 and Related Biomarkers
- Single-cell and spatial transcriptomics
- Cardiovascular Effects of Exercise
- RNA modifications and cancer
- Circadian rhythm and melatonin
- Spaceflight effects on biology
- Genetic Neurodegenerative Diseases
Altos Labs
2022-2025
Universitat Pompeu Fabra
2012-2024
Fleet Science Center
2024
Biomedical Research Networking Center on Neurodegenerative Diseases
2012-2023
Instituto de Investigación Biomédica de Málaga
2021
Centro de Investigación Biomédica en Red
2007-2017
Institute for Research in Biomedicine
2016
Instituto de Salud Carlos III
2014
Institució Catalana de Recerca i Estudis Avançats
2013-2014
University of Córdoba
1993-2010
Abstract The repair process of damaged tissue involves the coordinated activities several cell types in response to local and systemic signals. Following acute injury, infiltrating inflammatory cells resident stem orchestrate their restore homeostasis. However, during chronic damage, such as muscular dystrophies, inflammatory-cell infiltration fibroblast activation persists, while reparative capacity (satellite cells) is attenuated. Abnormal dystrophic muscle its end stage, fibrosis,...
Nerve activity controls fiber size and type in skeletal muscle, but the underlying molecular mechanisms remain largely unknown. We have previously shown that Ras–mitogen-activated protein kinase calcineurin control not regenerating rat muscle. Here we report constitutively active B (PKB), also known as Akt, increases prevents denervation atrophy adult muscles does affect profile. The coexistence of hypertrophic muscle fibers overexpressing activated PKB with normal-size untransfected within...
Abstract Tissue regeneration requires coordination between resident stem cells and local niche 1,2 . Here we identify that senescent are integral components of the skeletal muscle regenerative repress at all stages life. The technical limitation senescent-cell scarcity 3 was overcome by combining single-cell transcriptomics a enrichment sorting protocol. We identified isolated different cell types from damaged muscles young old mice. Deeper transcriptome, chromatin pathway analyses revealed...
Abstract Muscle atrophy and functional decline (sarcopenia) are common manifestations of frailty critical contributors to morbidity mortality in older people 1 . Deciphering the molecular mechanisms underlying sarcopenia has major implications for understanding human ageing 2 Yet, progress been slow, partly due difficulties characterizing skeletal muscle niche heterogeneity (whereby myofibres most abundant) obtaining well-characterized samples 3,4 Here we generate a...
A molecular clock network is crucial for daily physiology and maintaining organismal health. We examined the interactions importance of intratissue networks in muscle tissue maintenance. In arrhythmic mice showing premature aging, we created a basic module involving central peripheral (muscle) clock. Reconstituting brain-muscle sufficient to preserve fundamental homeostatic functions prevent aging. However, achieving whole requires contributions from other clocks. Mechanistically, acts as...
Nerve activity can induce long-lasting, transcription-dependent changes in skeletal muscle fibers and thus affect growth fiber-type specificity. Calcineurin signaling has been implicated the transcriptional regulation of slow fiber genes culture, but functional role calcineurin vivo not unambiguously demonstrated. Here, we report that up-regulation myosin heavy chain (MyHC) a MyHC-slow promoter induced by motor neurons regenerating rat soleus is prevented inhibitors cyclosporin A (CsA),...
In the fatal degenerative Duchenne muscular dystrophy (DMD), skeletal muscle is progressively replaced by fibrotic tissue. Here, we show that fibrinogen accumulates in dystrophic muscles of DMD patients and mdx mice. Genetic loss or pharmacological depletion these mice reduced fibrosis progression. Our results demonstrate fibrinogen–Mac-1 receptor binding, through induction IL-1β, drives synthesis transforming growth factor-β (TGFβ) macrophages, which turn induces collagen production...
Repair of damaged tissue requires the coordinated action inflammatory and tissue-specific cells to restore homeostasis, but underlying regulatory mechanisms are poorly understood. In this paper, we report new roles for MKP-1 (mitogen-activated protein kinase [MAPK] phosphatase-1) in controlling macrophage phenotypic transitions necessary appropriate muscle stem cell–dependent repair. By restricting p38 MAPK activation, allows early pro- antiinflammatory transition later progression into a...
Calcineurin (Cn) signaling has been implicated in nerve activity-dependent fiber type specification skeletal muscle, but the downstream effector pathway not established. We have investigated role of transcription factor nuclear activated T cells (NFAT), a major target Cn, by using an vivo transfection approach regenerating and adult rat muscles. NFAT transcriptional activity was monitored with two different NFAT-dependent reporters found to be higher slow compared fast is decreased...
A unique property of skeletal muscle is its ability to adapt mass changes in activity. Inactivity, as disuse or aging, causes atrophy, the loss and strength, leading physical incapacity poor quality life. Here, through a combination transcriptomics transgenesis, we identify sestrins, family stress-inducible metabolic regulators, protective factors against wasting. Sestrin expression decreases during inactivity genetic deficiency exacerbates wasting; conversely, sestrin overexpression...
Disruption of skeletal muscle homeostasis by substitution with fibrotic tissue constitutes the principal cause death in Duchenne muscular dystrophy (DMD) patients, yet implicated fibrogenic mechanisms remain poorly understood. This study identifies extracellular PAI-1/urokinase-type plasminogen activator (uPA) balance as an important regulator microribonucleic acid (miR)–21 biogenesis, controlling age-associated fibrosis and progression. Genetic loss PAI-1 mdx dystrophic mice anticipated...