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Updated: Jan 23, 2026
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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
Published on: April 6, 2022
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NAD+ metabolism controls inflammation during senescence
Timothy Nacarelli1, Rugang Zhang1
1Gene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA, USA.
Molecular & Cellular Oncology
|June 19, 2019
Summary
Nicotinamide adenine dinucleotide metabolism regulates the inflammatory senescence-associated secretory phenotype. This epigenetic-metabolic axis fuels cancer progression by altering senescent cell metabolism and inflammation.
Area of Science:
- Cellular senescence
- Epigenetics
- Metabolism
- Cancer biology
Background:
- Cellular senescence is a state of irreversible cell cycle arrest.
- Senescence-associated secretory phenotype (SASP) contributes to aging and cancer.
- The metabolic regulation of SASP is not fully understood.
Purpose of the Study:
- To investigate the role of nicotinamide adenine dinucleotide (NAD+) metabolism in controlling the pro-inflammatory SASP.
- To identify the key molecular players in the epigenetic-metabolic signaling axis regulating SASP.
Main Methods:
- Investigated NAD+ metabolism in senescent cells.
- Utilized molecular biology techniques to study high mobility group A (HMGA) and nicotinamide phosphoribosyltransferase (NAMPT).
- Assessed the impact of metabolic and epigenetic alterations on SASP and cancer progression.
Main Results:
- Discovered that NAD+ metabolism controls the pro-inflammatory SASP.
- Identified an epigenetic-metabolic signaling axis involving HMGA and NAMPT.
- Demonstrated that this axis drives metabolic changes and pro-inflammatory responses in senescent cells.
Conclusions:
- NAD+ metabolism is a critical regulator of the pro-inflammatory SASP.
- The HMGA-NAMPT axis represents a novel therapeutic target for modulating senescence and cancer progression.
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