Nature Search

Reply to “GDNF is not required for catecholaminergic neuron survival in vivo”

Alberto Pascual
José López-Barneo
Correspondence24 Feb 2015
Nature Neuroscience

Volume: 18, P: 322-323
Disruption of mitochondrial complex I induces progressive parkinsonism

Dysfunction of mitochondrial complex I in mice is sufficient to cause progressive parkinsonism in which the loss of nigral dopamine release critically contributes to motor dysfunction.

Patricia González-Rodríguez
Enrico Zampese
D. James Surmeier
Research03 Nov 2021
Nature

Volume: 599, P: 650-656
Hif1α-dependent mitochondrial acute O₂ sensing and signaling to myocyte Ca²⁺ channels mediate arterial hypoxic vasodilation

Hypoxia inhibits the activity of calcium channels in arterial myocytes by unknown mechanisms and contributes to arterial vasodilation. Here, the authors show that myocyte mitochondria are essential for sensing acute hypoxia and generate signals (NADH and H₂O₂) that modulate membrane calcium channels.

Alejandro Moreno-Domínguez
Olalla Colinas
José López-Barneo
ResearchOpen Access05 Aug 2024
Nature Communications

Volume: 15, P: 1-17
Author Correction: Disruption of mitochondrial complex I induces progressive parkinsonism

Patricia González-Rodríguez
Enrico Zampese
D. James Surmeier
Amendments and Corrections11 Feb 2022
Nature

Volume: 603, P: E1
Full protection from SARS-CoV-2 brain infection and damage in susceptible transgenic mice conferred by MVA-CoV2-S vaccine candidate

MVA-CoV2-S vaccination confers full protection against SARS-CoV-2 neuroinvasion in humanized mice, preventing brain viral replication and the associated neuronal and vascular damage, even after SARS-CoV-2 reinfection.

Javier Villadiego
Juan García-Arriaza
Juan José Toledo-Aral
Research09 Jan 2023
Nature Neuroscience

Volume: 26, P: 226-238
The role of Olfr78 in the breathing circuit of mice

Hortensia Torres-Torrelo
Patricia Ortega-Sáenz
José López-Barneo
Research26 Sept 2018
Nature

Volume: 561, P: E33-E40
Publisher Correction: Cellular adaptation to oxygen deficiency beyond the Nobel award

José López-Barneo
M. Celeste Simon
Amendments and CorrectionsOpen Access25 Feb 2020
Nature Communications

Volume: 11, P: 1
Hypoxia compromises the mitochondrial metabolism of Alzheimer’s disease microglia via HIF1

Microglia can help clear amyloid β plaques in the Alzheimer’s disease brain but may also become dysfunctional and can contribute to disease progression. March-Diaz et al. reveal that hypoxia, a potentially modifiable risk factor for Alzheimer’s disease, disrupts the metabolism and function of microglia near plaques, which may contribute to neuropathology.

Rosana March-Diaz
Nieves Lara-Ureña
Alberto Pascual
Research15 Apr 2021
Nature Aging

Volume: 1, P: 385-399
Low glucose–sensing cells in the carotid body

Ricardo Pardal
José López-Barneo
Research19 Feb 2002
Nature Neuroscience

Volume: 5, P: 197-198
Transgenic NADH dehydrogenase restores oxygen regulation of breathing in mitochondrial complex I-deficient mice

Activation of breathing during hypoxia is abolished in mice lacking mitochondrial complex I in carotid body chemoreceptors, however the specific contribution of mitochondrial complex I to this process is unclear. Here, the authors show that recovery of NADH dehydrogenase activity, but not proton pumping, by transgenic expression of a yeast enzyme rescues cellular and systemic sensitivity to changes in O2 tension.

Blanca Jiménez-Gómez
Patricia Ortega-Sáenz
José López-Barneo
ResearchOpen Access01 Mar 2023
Nature Communications

Volume: 14, P: 1-14
Absolute requirement of GDNF for adult catecholaminergic neuron survival

The exact function of glial cell line–derived neurotrophic factor (GDNF) in catecholaminergic cell survival in adulthood is unclear. Using a conditional GDNF-null mouse that suppresses GDNF expression in adulthood, Pascual et al. show that GDNF is an essential factor whose downregulation results in massive catecholaminergic neuronal death. Carlos Ibáñez discusses this paper in an accompanying News and Views.

Alberto Pascual
María Hidalgo-Figueroa
José López-Barneo
Research08 Jun 2008
Nature Neuroscience

Volume: 11, P: 755-761
Microglia mitochondrial complex I deficiency during development induces glial dysfunction and early lethality

Microglia rely on mitochondrial complex I during development, suggesting that complex I deficiency in microglia may have a role in primary mitochondrial diseases.

Bella Mora-Romero
Nicolas Capelo-Carrasco
Alberto Pascual
Research24 Jul 2024
Nature Metabolism

Volume: 6, P: 1479-1491
Direct confocal acquisition of fluorescence from X-gal staining on thick tissue sections

Konstantin L. Levitsky
Juan José Toledo-Aral
Javier Villadiego
ResearchOpen Access14 Oct 2013
Scientific Reports

Volume: 3, P: 1-6
Lactate sensing mechanisms in arterial chemoreceptor cells

Lactate levels in blood change during hypoxia or exercise, however whether this variable is sensed to evoke adaptive responses is unknown. Here the authors show that oxygen-sensing carotid body cells stimulated by hypoxia are also activated by lactate to potentiate a compensatory ventilatory response.

Hortensia Torres-Torrelo
Patricia Ortega-Sáenz
José López-Barneo
ResearchOpen Access06 Jul 2021
Nature Communications

Volume: 12, P: 1-13
Mitochondrial integrated stress response controls lung epithelial cell fate

This study highlights the role of mitochondrial complex I-dependent NAD⁺ regeneration in directing lung epithelial cell fate during postnatal alveolar development by preventing pathological integrated stress response induction.

SeungHye Han
Minho Lee
Navdeep S. Chandel
ResearchOpen Access09 Aug 2023
Nature

Volume: 620, P: 890-897
Genetic map of the carotid body stem cell niche with focus on the O₂-sensing chemoreceptor cell lineage

Ana Santamaría-Santiago
Verónica Sobrino
Ricardo Pardal
ResearchOpen Access28 Jul 2025
Scientific Reports

Volume: 15, P: 1-17
Na⁺ controls hypoxic signalling by the mitochondrial respiratory chain

Na⁺ controls the function of the mitochondrial oxidative phosphorylation system and hypoxic redox signalling through an unexpected interaction with phospholipids.

Pablo Hernansanz-Agustín
Carmen Choya-Foces
Antonio Martínez-Ruiz
Research29 Jul 2020
Nature

Volume: 586, P: 287-291
Cellular adaptation to oxygen deficiency beyond the Nobel award

Understanding the cellular adaptation to oxygen deficiency -hypoxia- has a profound impact on our knowledge of the pathogenesis of several diseases. The elucidation of the molecular machinery that regulates response to hypoxia has been awarded the Nobel Prize in Physiology or Medicine.

José López-Barneo
M. Celeste Simon
Comments & OpinionOpen Access30 Jan 2020
Nature Communications

Volume: 11, P: 1-3
Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice

Gregory S. McElroy
Ram P. Chakrabarty
Navdeep S. Chandel
ResearchOpen Access25 Mar 2022
Scientific Reports

Volume: 12, P: 1-15
Author Correction: Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice

Gregory S. McElroy
Ram P. Chakrabarty
Navdeep S. Chandel
Amendments and CorrectionsOpen Access17 May 2022
Scientific Reports

Volume: 12, P: 1-2

Search

Reply to “GDNF is not required for catecholaminergic neuron survival in vivo”

Disruption of mitochondrial complex I induces progressive parkinsonism

Hif1α-dependent mitochondrial acute O₂ sensing and signaling to myocyte Ca²⁺ channels mediate arterial hypoxic vasodilation

Author Correction: Disruption of mitochondrial complex I induces progressive parkinsonism

Full protection from SARS-CoV-2 brain infection and damage in susceptible transgenic mice conferred by MVA-CoV2-S vaccine candidate

The role of Olfr78 in the breathing circuit of mice

Publisher Correction: Cellular adaptation to oxygen deficiency beyond the Nobel award

Hypoxia compromises the mitochondrial metabolism of Alzheimer’s disease microglia via HIF1

Low glucose–sensing cells in the carotid body

Transgenic NADH dehydrogenase restores oxygen regulation of breathing in mitochondrial complex I-deficient mice

Absolute requirement of GDNF for adult catecholaminergic neuron survival

Microglia mitochondrial complex I deficiency during development induces glial dysfunction and early lethality

Direct confocal acquisition of fluorescence from X-gal staining on thick tissue sections

Lactate sensing mechanisms in arterial chemoreceptor cells

Mitochondrial integrated stress response controls lung epithelial cell fate

Genetic map of the carotid body stem cell niche with focus on the O₂-sensing chemoreceptor cell lineage

Na⁺ controls hypoxic signalling by the mitochondrial respiratory chain

Cellular adaptation to oxygen deficiency beyond the Nobel award

Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice

Author Correction: Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice

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