AI Article Synopsis
- Aging leads to disruptions in biological balance, prompting the need for comprehensive studies on molecular changes over time.
- Research using mouse liver data reveals that various lifespan-extending methods (like acarbose, 17α-estradiol, rapamycin, and calorie restriction) generally improve the regulation of biological functions, particularly in areas like fatty acid oxidation and immune responses.
- The study emphasizes the effectiveness of systems-level approaches in uncovering the complex processes that contribute to aging and potential longevity interventions.
Article Abstract
Aging manifests as progressive deteriorations in homeostasis, requiring systems-level perspectives to investigate the gradual molecular dysregulation of underlying biological processes. Here, we report systemic changes in the molecular regulation of biological processes under multiple lifespan-extending interventions. Differential Rank Conservation (DIRAC) analyses of mouse liver proteomics and transcriptomics data show that mechanistically distinct lifespan-extending interventions (acarbose, 17α-estradiol, rapamycin, and calorie restriction) generally tighten the regulation of biological modules. These tightening patterns are similar across the interventions, particularly in processes such as fatty acid oxidation, immune response, and stress response. Differences in DIRAC patterns between proteins and transcripts highlight specific modules which may be tightened via augmented cap-independent translation. Moreover, the systemic shifts in fatty acid metabolism are supported through integrated analysis of liver transcriptomics data with a mouse genome-scale metabolic model. Our findings highlight the power of systems-level approaches for identifying and characterizing the biological processes involved in aging and longevity.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363145 | PMC |
| http://dx.doi.org/10.1038/s42003-023-05128-y | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Chaperone-mediated autophagy as a modulator of aging and longevity.
Front Aging
December 2024
Department of Pathology, University of New Mexico Health Sciences Center, Albuquerque, NM, United States.
Chaperone-mediated autophagy (CMA) is the lysosomal degradation of individually selected proteins, independent of vesicle fusion. CMA is a central part of the proteostasis network in vertebrate cells. However, CMA is also a negative regulator of anabolism, and it degrades enzymes required for glycolysis, lipogenesis, and translation at the cytoplasmic ribosome.
View Article and Find Full Text PDFDownregulation of the NF-κB protein p65 is a shared phenotype among most anti-aging interventions.
Geroscience
December 2024
Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI, USA.
Many aspects of inflammation increase with aging in mice and humans. Transcriptomic analysis revealed that many murine anti-aging interventions produce lower levels of pro-inflammatory proteins. Here, we explore the hypothesis that different longevity interventions diminish NF-κB levels, potentially mediating some of the anti-inflammatory benefits of lifespan-extending interventions.
View Article and Find Full Text PDFNegative effects of lifespan extending intervention on resilience in mice.
PLoS One
November 2024
Department of Biology, University of Alabama at Birmingham, Birmingham, AL, United States of America.
One key goal of basic aging research is the development of reliable assays of both current and future health. These assays could dramatically accelerate progress toward developing health-extending interventions by obviating the need for full lifespan studies, especially if they were informative relatively early in life. One potential approach is the assessment of physiological resilience, defined as the ability to recover from an adverse event.
View Article and Find Full Text PDFTemperature-dependent lifespan extension is achieved in miR-80-deleted Caenorhabditis elegans by NLP-45 to modulate endoplasmic reticulum unfolded protein responses.
Aging Cell
September 2024
State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Article Synopsis
- MicroRNA, specifically miR-80, is important for regulating gene expressions related to aging, but the exact processes are still not fully understood.
- In experiments with Caenorhabditis elegans, the absence of miR-80 extended lifespan at lower temperatures (20°C) by increasing the expression of NLP-45, which is linked to longevity.
- However, at higher temperatures (25°C), the expected lifespan extension did not occur due to changes in miR-80 levels, suggesting that environmental factors can influence these molecular regulatory networks involved in aging.
Consolidating multiple evolutionary theories of ageing suggests a need for new approaches to study genetic contributions to ageing decline.
Ageing Res Rev
September 2024
Ohio Musculoskeletal and Neurological Institute, Heritage College of Osteopathic Medicine, Athens, OH 45701, United States. Electronic address:
Understanding mechanisms of ageing remains a complex challenge for biogerontologists, but recent adaptations of evolutionary ageing theories offer a compelling lens in which to view both age-related molecular and physiological deterioration. Ageing is commonly associated with progressive declines in biochemical and molecular processes resulting from damage accumulation, yet the role of continued developmental gene activation is less appreciated. Natural selection pressures are at their highest in youthful periods to modify gene expression towards maximising reproductive capacity.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!