Vincenzo Sorrentino

Assistant Prof.

National University Singapore Yong Loo Lin School of Medicine

Singapore

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About

Vincenzo Sorrentino is an Assistant Professor at the National University of Singapore Yong Loo Lin School of Medicine. His research focuses on NAD+ metabolism, aging, and chronic kidney disease, as well as the intersection of biotechnology and geroscience for promoting healthy longevity. Recent publications include studies on mitochondrial function, metabolic landscapes in chronic kidney disease, and the role of nicotinamide riboside in muscle regeneration.

Articles (13)

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2025

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2024

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2024

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2024

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2024

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2024

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2023

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2022

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2022

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2022

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2022

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2021

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2021

Collaborators (11)

Anja Groth

Københavns Universitet

DENMARK

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Takashi Nakagawa

Professor

University of Toyama

JAPAN

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Sabrina Büttner

Associate Professor

Stockholm University

SWEDEN

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D. Sean Froese

SWITZERLAND

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Alessandra Tammaro

University of Amsterdam

NETHERLANDS

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Estéfano Pinilla

Aarhus University

DENMARK

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Jonas Treebak

Københavns Universitet

DENMARK

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Alexandra Stolzing

Loughborough University

UNITED KINGDOM

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Fabian Finger

Assistant Professor

University of Copenhagen

DENMARK

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Thomas Rando

Professor

University of California

UNITED STATES

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Traian Popa

Lausanne University Hospital

SWITZERLAND

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Vincenzo Sorrentino

Research Interests

Contact this professor

About

Articles (13)

The role of NAD+ metabolism and its modulation of mitochondria in aging and disease

Trigonelline is an NAD+ precursor that improves muscle function during ageing and is reduced in human sarcopenia

Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity.

Impaired renal transporter gene expression and uremic toxin excretion as aging hallmarks in cats with naturally occurring chronic kidney disease

Metabolic Landscape of Naturally Occurring CKD in Cats: An Integrated Multiomics Study

Towards Healthy Longevity: Comprehensive Insights from Molecular Targets and Biomarkers to Biological Clocks

The mitochondrial calcium uniporter (MCU) activates mitochondrial respiration and enhances mobility by regulating mitochondrial redox state

NAD+ Metabolism and Interventions in Premature Renal Aging and Chronic Kidney Disease

Elucidation of Amyloid-Beta's Gambit in Oligomerisation:Truncated Aβ fragments of residues Aβ1-23, Aβ1-24 and Aβ1-25 rapidly seed to form SDS-stable, low molecular weight Aβ oligomers that impair synaptic plasticity

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

Boosting mitochondrial health to counteract neurodegeneration

Mitochondrial disease, mitophagy, and cellular distress in methylmalonic acidemia.

NAD+ boosting reduces age-associated amyloidosis and restores mitochondrial homeostasis in muscle.

Collaborators (11)

Anja Groth

Takashi Nakagawa

Sabrina Büttner

D. Sean Froese

Alessandra Tammaro

Estéfano Pinilla

Jonas Treebak

Alexandra Stolzing

Fabian Finger

Thomas Rando

Traian Popa

Make your next move.

Vincenzo Sorrentino

Research Interests

Contact this professor

About

Articles (13)

The role of NAD+ metabolism and its modulation of mitochondria in aging and disease

Trigonelline is an NAD+ precursor that improves muscle function during ageing and is reduced in human sarcopenia

Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity.

Impaired renal transporter gene expression and uremic toxin excretion as aging hallmarks in cats with naturally occurring chronic kidney disease

Metabolic Landscape of Naturally Occurring CKD in Cats: An Integrated Multiomics Study

Towards Healthy Longevity: Comprehensive Insights from Molecular Targets and Biomarkers to Biological Clocks

The mitochondrial calcium uniporter (MCU) activates mitochondrial respiration and enhances mobility by regulating mitochondrial redox state

NAD+ Metabolism and Interventions in Premature Renal Aging and Chronic Kidney Disease

Elucidation of Amyloid-Beta's Gambit in Oligomerisation:Truncated A&beta; fragments of residues A&beta;1-23, A&beta;1-24 and A&beta;1-25 rapidly seed to form SDS-stable, low molecular weight A&beta; oligomers that impair synaptic plasticity

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

Boosting mitochondrial health to counteract neurodegeneration

Mitochondrial disease, mitophagy, and cellular distress in methylmalonic acidemia.

NAD+ boosting reduces age-associated amyloidosis and restores mitochondrial homeostasis in muscle.

Collaborators (11)

Anja Groth

Takashi Nakagawa

Sabrina Büttner

D. Sean Froese

Alessandra Tammaro

Estéfano Pinilla

Jonas Treebak

Alexandra Stolzing

Fabian Finger

Thomas Rando

Traian Popa

Make your next move.

Elucidation of Amyloid-Beta's Gambit in Oligomerisation:Truncated Aβ fragments of residues Aβ1-23, Aβ1-24 and Aβ1-25 rapidly seed to form SDS-stable, low molecular weight Aβ oligomers that impair synaptic plasticity