Carlos Canto Alvarez

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PURPOSE OF REVIEW: Peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC-1alpha) has been extensively described as a master regulator of mitochondrial biogenesis. However, PGC-1alpha activity is not constant and can be finely tuned in r ...

Neuromuscular diseases are often caused by inherited mutations that lead to progressive skeletal muscle weakness and degeneration. In diverse populations of normal healthy mice, we observed correlations between the abundance of mRNA transcripts related to ...

Nicotinamide riboside kinases (NRKs) control the conversion of dietary Nicotinamide Riboside (NR) to NAD(+), but little is known about their contribution to endogenous NAD(+) turnover and muscle plasticity during skeletal muscle growth and remodeling. Usin ...

Nicotinamide adenine dinucleotide (NAD(+)) and its reduced form (NADH) are coenzymes employed in hundreds of metabolic reactions. NAD(+) also serves as a substrate for enzymes such as sirtuins, poly(ADP-ribose) polymerases (PARPs) and ADP-ribosyl cyclases. ...

Mitochondria constantly undergo fusion and fission events, referred as mitochondrial dynamics, which determine mitochondrial architecture and bioenergetics. Cultured cell studies demonstrate that mitochondrial dynamics are acutely regulated by phosphorylat ...

Objective: A decay in intracellular NAD(+) levels is one of the hallmarks of physiological decline in normal tissue functions. Accordingly, dietary supplementation with NAD(+) precursors can prevent, alleviate, or even reverse multiple metabolic complicati ...

It has been recently shown that increased oxidative phosphorylation, as reflected by increased mitochondrial activity, together with impairment of the mitochondrial stress response, can severely compromise hematopoietic stem cell (HSC) regeneration. Here w ...

Circadian rhythms provide a selective advantage by anticipating organismal nutrient needs and guaranteeing optimal metabolic capacity during active hours. Impairment of circadian rhythms is associated with increased risk of type 2 diabetes and emerging evi ...

NAD(+) is a vital redox cofactor and a substrate required for activity of various enzyme families, including sirtuins and poly(ADP-ribose) polymerases. Supplementation with NAD(+) precursors, such as nicotinamide mononucleotide (NMN) or nicotinamide ribosi ...

Despite their classic bean-shaped depiction, mitochondria have very different aspects in each cell type. From long filamentous structures to punctuated small round organelles. These shapes can dynamically change in response to nutrients and in situations o ...

Objective: Disturbances in NAD+ metabolism have been described as a hallmark for multiple metabolic and age-related diseases, including type 2 diabetes. While alterations in pancreatic (3-cell function are critical determinants of whole-body glucose homeos ...

The last decade has seen a strong proliferation of therapeutic strategies for the treatment of metabolic and age-related diseases based on increasing cellular NAD(+) bioavailability. Among them, the dietary supplementation with NAD(+) precursors-classicall ...

Dietary restriction can extend life span in most organisms tested to date, suggesting that mechanisms sensing nutrient and energy availability might regulate longevity. The AMP-activated protein kinase (AMPK) has emerged as a key energy sensor with the abi ...

Transcriptional coregulators control the activity of many transcription factors and are thought to have wide-ranging effects on gene expression patterns. We show here that muscle-specific loss of nuclear receptor corepressor 1 (NCoR1) in mice leads to enha ...

Through evolution, eukaryote organisms have developed the ability to use different molecules as independent precursors to generate nicotinamide adenine dinucleotide (NAD(+)), an essential molecule for life. However, whether these different precursors act i ...

Mitochondrial dysfunction is a hallmark of multiple metabolic complications. Physical activity is known to increase mitochondrial content in skeletal muscle, counteracting age-related decline in muscle function and protecting against metabolic and cardiova ...

We previously demonstrated that the deletion of the poly(ADP-ribose) polymerase (Parp)-1 gene in mice enhances oxidative metabolism, thereby protecting against diet-induced obesity. However, the therapeutic use of PARP inhibitors to enhance mitochondrial f ...

Alterations in cellular nicotinamide adenine dinucleotide (NAD(+)) levels have been observed in multiple lifestyle and age-related medical conditions. This has led to the hypothesis that dietary supplementation with NAD(+) precursors, or vitamin B3s, could ...

A century after the identification of a coenzymatic activity for NAD(+), NAD(+) metabolism has come into the spotlight again due to the potential therapeutic relevance of a set of enzymes whose activity is tightly regulated by the balance between the oxidi ...

During fasting and after exercise, skeletal muscle efficiently switches from carbohydrate to lipid as the main energy source to preserve glycogen stores and blood glucose levels for glucose-dependent tissues. Skeletal muscle cells sense this limitation in ...

Carlos Canto Alvarez

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PGC-1alpha, SIRT1 and AMPK, an energy sensing network that controls energy expenditure

NAD(+) repletion improves muscle function in muscular dystrophy and counters global PARylation

Nicotinamide riboside kinases regulate skeletal muscle fiber-type specification and are rate-limiting for metabolic adaptations during regeneration

A Method to Monitor the NAD(+) Metabolome-From Mechanistic to Clinical Applications

Crosstalk between Drp1 phosphorylation sites during mitochondrial remodeling and their impact on metabolic adaptation

A reduced form of nicotinamide riboside defines a new path for NAD(+) biosynthesis and acts as an orally bioavailable NAD(+) precursor

The NAD-Booster Nicotinamide Riboside Potently Stimulates Hematopoiesis through Increased Mitochondrial Clearance

Circadian Rhythms and Mitochondria: Connecting the Dots

NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cells

Mitochondrial Dynamics: Shaping Metabolic Adaptation

Nicotinamide riboside kinase 1 protects against diet and age-induced pancreatic (3-cell failure

NAD(+) Precursors: A Questionable Redundancy

Calorie restriction: is AMPK a key sensor and effector?

NCoR1 Is a Conserved Physiological Modulator of Muscle Mass and Oxidative Function

Nicotinamide Riboside and Dihydronicotinic Acid Riboside Synergistically Increase Intracellular NAD(+) by Generating Dihydronicotinamide Riboside

Enhanced Respiratory Chain Supercomplex Formation in Response to Exercise in Human Skeletal Muscle

Pharmacological Inhibition of Poly(ADP-Ribose) Polymerases Improves Fitness and Mitochondrial Function in Skeletal Muscle

Balancing NAD(+) deficits with nicotinamide riboside: therapeutic possibilities and limitations

The Secret Life of NAD+: An Old Metabolite Controlling New Metabolic Signaling Pathways

Interdependence of AMPK and SIRT1 for Metabolic Adaptation to Fasting and Exercise in Skeletal Muscle