Nora Hernández-Montalvo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Nora Hernández-Montalvo has a total of 22 co-authors. Here are the top co-authors by number of shared publications:
- Abraham Acevedo-Arozena
Hospital Universitario de Canarias
2 shared publications - Sonia Alonso-Martin
Center for Biomedical Network Research on Neurodegenerative Diseases (CIBERNED), Carlos III Health Institute, Spain
2 shared publications Adolfo Lopez de Munain
Biodonostia Institute
1 shared publication- Adolfo López de Munain
CIBERNED, ISCIII (CIBER, Carlos III Institute, Spanish Ministry of Sciences and Innovation), Madrid, Spain
1 shared publication Ainhoa Vidal-Gil
Stem Cells and Aging Group, Bioengineering Area, Biogipuzkoa Health Research Institute
1 shared publication- Ainhoa Vidal-Gil
Stem Cells and Aging Group, Bioengineering Area, Biogipuzkoa Health Research Institute, Donostia/San Sebastián, Spain
1 shared publication
Latest Publications
- Open Access
- 12 August 2026
- Published by Springer Nature in Research Square
TDP-43 loss drives premature aging and regenerative failure in skeletal muscle stem cells
TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of amyotrophic lateral sclerosis (ALS) and related disorders, yet its role in skeletal muscle stem cells, the satellite cells (SC), remains incompletely understood. Here, we investigated ALS-associated gain- and loss-of-function TDP-43 mutations together with inducible SC-specific TDP-43 deletion. While TDP-43Q331K and heterozygous TDP-43F210I mice displayed normal muscle homeostasis, SC abundance, and regenerative capacity, complete TDP-43 loss caused a marked reduction of the SC pool, particularly in females, and shifted SCs from a CD34high stem-like state toward a CD34low primed population. TDP-43-deficient SCs failed to clonally expand, proliferate, and differentiate, resulting in severe regenerative failure following muscle injury. Notably, the SC pool failed to recover after injury and was nearly depleted 30 days post-injury, accompanied by muscle loss, fibrosis and fat infiltration. Transcriptomic analyses revealed activation of stress and aging-associated programs in uninjured TDP-43-deficient SCs, indicating the premature acquisition of an aging-like state. Consistently, chronological aging further exacerbated SC depletion, establishing TDP-43 as a critical regulator of SC stemness, regeneration, and resistance to age-related decline.
- 12 August 2026
- Published by Springer Nature in Research Square
Open AccessTDP-43 loss drives premature aging and regenerative failure in skeletal muscle stem cells
TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of amyotrophic lateral sclerosis (ALS) and related disorders, yet its role in skeletal muscle stem cells, the satellite cells (SC), remains incompletely understood. Here, we investigated ALS-associated gain- and loss-of-function TDP-43 mutations together with inducible SC-specific TDP-43 deletion. While TDP-43Q331K and heterozygous TDP-43F210I mice displayed normal muscle homeostasis, SC abundance, and regenerative capacity, complete TDP-43 loss caused a marked reduction of the SC pool, particularly in females, and shifted SCs from a CD34high stem-like state toward a CD34low primed population. TDP-43-deficient SCs failed to clonally expand, proliferate, and differentiate, resulting in severe regenerative failure following muscle injury. Notably, the SC pool failed to recover after injury and was nearly depleted 30 days post-injury, accompanied by muscle loss, fibrosis and fat infiltration. Transcriptomic analyses revealed activation of stress and aging-associated programs in uninjured TDP-43-deficient SCs, indicating the premature acquisition of an aging-like state. Consistently, chronological aging further exacerbated SC depletion, establishing TDP-43 as a critical regulator of SC stemness, regeneration, and resistance to age-related decline.
- Open Access
Loss of TDP-43 drives premature aging and impairs skeletal muscle stem cell pool restoration
TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of amyotrophic lateral sclerosis (ALS) and related disorders, yet its role in skeletal muscle stem cells, the satellite cells (SC), remains incompletely understood. Here, we investigated ALS-associated gain- and loss-of-function TDP-43 mutations together with inducible SC-specific TDP-43 deletion. While TDP-43 Q331K and heterozygous TDP-43 F210I mice displayed normal muscle homeostasis, SC abundance, and regenerative capacity, complete TDP-43 loss caused a marked reduction of the SC pool, particularly in females, and shifted SCs from a CD34 high stem-like state toward a CD34 low primed population. TDP-43-deficient SCs failed to clonally expand, proliferate, and differentiate, resulting in severe regenerative failure following muscle injury. Notably, the SC pool failed to recover after injury and was nearly depleted 30 days post-injury, accompanied by muscle loss, fibrosis and fat infiltration. Transcriptomic analyses revealed activation of stress and aging-associated programs in uninjured TDP-43-deficient SCs, indicating the premature acquisition of an aging-like state. Consistently, chronological aging further exacerbated SC depletion, establishing TDP-43 as a critical regulator of SC stemness, regeneration, and resistance to age-related decline.
Open AccessLoss of TDP-43 drives premature aging and impairs skeletal muscle stem cell pool restoration
TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of amyotrophic lateral sclerosis (ALS) and related disorders, yet its role in skeletal muscle stem cells, the satellite cells (SC), remains incompletely understood. Here, we investigated ALS-associated gain- and loss-of-function TDP-43 mutations together with inducible SC-specific TDP-43 deletion. While TDP-43 Q331K and heterozygous TDP-43 F210I mice displayed normal muscle homeostasis, SC abundance, and regenerative capacity, complete TDP-43 loss caused a marked reduction of the SC pool, particularly in females, and shifted SCs from a CD34 high stem-like state toward a CD34 low primed population. TDP-43-deficient SCs failed to clonally expand, proliferate, and differentiate, resulting in severe regenerative failure following muscle injury. Notably, the SC pool failed to recover after injury and was nearly depleted 30 days post-injury, accompanied by muscle loss, fibrosis and fat infiltration. Transcriptomic analyses revealed activation of stress and aging-associated programs in uninjured TDP-43-deficient SCs, indicating the premature acquisition of an aging-like state. Consistently, chronological aging further exacerbated SC depletion, establishing TDP-43 as a critical regulator of SC stemness, regeneration, and resistance to age-related decline.