Mitochondrial Dysfunction-Induced Senescence Model Customization Services

Dysfunctional mitochondria accumulate with age, best documented in tissues comprised largely of post-mitotic cells (e.g., muscle cells and neurons). One consequence of mitochondrial dysfunction is cellular senescence, a complex stress response by which proliferative cells permanently lose the ability to divide. The robust mitochondrial dysfunction-induced senescence model is constructed to help researchers investigate the molecular mechanisms, contributing to a deeper understanding of age-related diseases and potential therapeutic interventions.

Fig. 1 Comparison between mitochondrial dysfunction associated-senescence (MiDAS) and stress-induced senescence. (Gallage S and Gil J, 2016)

At CD BioSciences, we specialize in providing customization services for mitochondrial dysfunction-induced senescence models. With years of experience in the industry, our team of expert biologists and advanced technologies enable us to offer comprehensive analysis services for mitochondrial dysfunction and senescent phenotypes.

How Do We Construct Mitochondrial Dysfunction-Induced Senescence Models?

Cell line selection

We guide our clients to choose suitable cell lines for constructing mitochondrial dysfunction-induced senescence models. Depending on the specific research interests, consider cell lines with relevant characteristics, such as human fibroblasts or epithelial cells.

Induction of mitochondrial dysfunction

We help clients select appropriate mitochondrial toxins, such as rotenone, antimycin A, or oligomycin, to induce mitochondrial dysfunction. We employ these toxins in the construction of the cellular model, considering the concentrations, exposure durations, and potential downstream effects on cellular physiology.

Assessment of mitochondrial dysfunction

We employ a range of techniques to evaluate mitochondrial function and dysfunction in the cellular models. Our services include measurements of mitochondrial membrane potential, ATP production, reactive oxygen species (ROS) levels, mitochondrial DNA damage, and alterations in mitochondrial morphology.

Characterization of senescent phenotypes

We perform a comprehensive characterization of the senescent phenotype to validate the cellular models, such as assessing senescence-associated beta-galactosidase (SA-β-gal) activity, cell cycle arrest, senescence-associated secretory phenotype (SASP), and alterations in gene expression profiles associated with senescence.

Optimization of aging models

If requested, we also help clients carry out our iterative optimization steps to refine the cellular models, ensuring their stability, reproducibility, and relevance to your specific research needs.

Extensive Applications of Mitochondrial Dysfunction-Induced Senescence Models

• Mechanistic studies. Our complete services assist clients in elucidating the signaling pathways, regulatory networks, and molecular interactions involved in MiDAS, which can reveal the fundamental biology of mitochondria and cellular aging.
• Disease modeling. Mitochondrial dysfunction is implicated in a wide range of diseases, including neurodegenerative disorders, metabolic syndromes, cardiovascular diseases, and cancer. We help clients customize mitochondrial dysfunction-induced senescence models as platforms to investigate the role of mitochondrial dysfunction in disease pathogenesis and progression
• Drug discovery and development. Using mitochondrial dysfunction-induced senescence models, our clients can identify novel therapeutic agents and optimize treatment strategies for aging-related diseases and conditions associated with mitochondrial dysfunction.

Our Service Features

• Customization and flexibility
• Timely project execution
• Confidentiality and data security

CD BioSciences offers comprehensive customization services for mitochondrial dysfunction-induced senescence models, supported by our expertise, advanced technologies, and commitment to delivering high-quality results. If you are interested in our services, please feel free to contact us or make an online inquiry.

Reference

1. Gallage S and Gil J. Mitochondrial dysfunction meets senescence. Trends in Biochemical Sciences, 2016, 41 (3): 207-209.