Mitochondrial Dysfunction Mechanism Research Service

Introduction Services Measurements Advantages Inquiry Workflow FAQs Published Data

Introduction

Mitochondrial dysfunction refers to the impairment of mitochondrial function, which plays a crucial role in cellular energy production, metabolism, and overall cellular health. Mitochondria are responsible for generating ATP through oxidative phosphorylation and regulating key cellular processes such as apoptosis, calcium homeostasis, and reactive oxygen species (ROS) production. Dysfunctional mitochondria can lead to reduced ATP production, increased oxidative stress, and disrupted cellular signaling, contributing to the development of various diseases and aging processes. Mitochondrial dysfunction can be classified into two main types: primary dysfunction, which arises from genetic mutations affecting mitochondrial DNA (mtDNA) or nuclear genes involved in mitochondrial function, and secondary dysfunction, caused by environmental factors such as oxidative damage, toxins, or metabolic disorders. Creative Biolabs offers specialized services to study the mechanisms of mitochondrial dysfunction using a variety of in vitro and in vivo models. These models help evaluate mitochondrial biogenesis, bioenergetics, ROS production, and mitochondrial dynamics. Our scientific team provides in-depth analysis, guiding the development of potential therapeutic strategies to mitigate the effects of mitochondrial dysfunction.

Services

Creative Biolabs offers a wide range of well-established in vitro and in vivo models for studying the mechanisms of mitochondrial dysfunction. Our models focus on various aspects of mitochondrial dysfunction, including impaired mitochondrial bioenergetics, increased reactive oxygen species (ROS) production, and disturbances in mitochondrial dynamics and mitophagy. These models are designed to closely replicate human cellular and tissue physiology, enabling detailed evaluations of the impact of various factors, including oxidative stress and genetic mutations, on mitochondrial function. To learn more about our available models for studying the mechanisms of mitochondrial dysfunction, please explore the links b elow.

Mitochondrial Autophagy Research

Mitochondrial Morphology/Distribution Research

Mitochondrial Respiratory Chain Research

Mitochondrial Membrane Potential Research

Mitochondrial Membrane Permeability Transition Pore Research

Fig.1 Diagram showing the mitochondrial structure, function, and aging-related changes. (OA Literature) Fig. 1 Mitochondrial structure, function, and aging-related changes.¹

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Measurements

We offer a range of advanced measurements for evaluating mitochondrial dysfunction, utilizing cutting-edge technologies to investigate various aspects of mitochondrial health. Our evaluation includes, but is not limited to:

General Observations: Cell viability, ATP production levels, mitochondrial membrane potential, and ROS generation.
Mitochondrial Bioenergetics: Measurement of oxygen consumption rates (OCR) and extracellular acidification rates (ECAR) to assess mitochondrial function using Seahorse XF technology.
Immunohistochemistry: Detection of mitochondrial markers (e.g., TOM20, COX IV) to evaluate mitochondrial integrity and distribution in tissue samples.
Cytokine Profiling (e.g., ELISA): Analysis of pro-inflammatory mediators like TNF-α, IL-6, and IL-1β to evaluate the inflammatory response induced by mitochondrial dysfunction.
Mitochondrial Dynamics Analysis: Assessment of mitochondrial fission and fusion processes using specific markers (e.g., Drp1, Mfn2) and imaging techniques (e.g., live cell imaging).
Gene/Protein Expression Profiling: RT-qPCR and Western blotting to quantify the expression of key mitochondrial genes and proteins involved in oxidative phosphorylation, biogenesis (e.g., PGC-1α), and mitophagy (e.g., Parkin).

In addition to our established models of mitochondrial dysfunction, our expertise extends to the development of novel animal models tailored to meet specific research needs, guided by current literature and prior studies. Our scientific team is available to assist in experimental design, model selection, and data analysis, ensuring a personalized and effective approach to your project at every stage.

Advantages

1. Expertise in Mitochondrial Dysfunction Research

We specialize in the study of mitochondrial dysfunction, offering in-depth knowledge and advanced models to investigate mitochondrial bioenergetics, oxidative stress, and dynamics. Our expertise helps provide reliable insights into the mechanisms driving diseases related to mitochondrial dysfunction.

2. Comprehensive Model Systems

Our in vitro and in vivo models replicate human mitochondrial physiology, enabling accurate evaluations of mitochondrial dysfunction under various conditions. We offer a wide range of models for assessing mitochondrial health, from cellular models to whole-organism studies.

3. Custom Research Solutions

Every project is unique. Our team collaborates closely with you to develop customized research strategies and select the best models for your specific study. Whether you are examining drug effects, genetic mutations, or environmental stressors, we tailor our approach to meet your research goals.

4. State-of-the-Art Technology

We employ cutting-edge technologies such as Seahorse XF for mitochondrial bioenergetics, advanced microscopy for mitochondrial dynamics, and high-sensitivity ELISA for cytokine profiling. These tools ensure the highest quality and precision in your data collection.

5. Rigorous Quality Assurance

All our models and methodologies undergo thorough validation to ensure consistency and reproducibility. Our commitment to high-quality, scientifically rigorous research ensures that your project is based on reliable data that supports meaningful outcomes.

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Workflow

Fig 3. Workflow of Creative Biolabs service. (Creative Biolabs Original)

FAQs

What services do you offer?

We offer specialized in vitro and in vivo models for studying mitochondrial dysfunction, including bioenergetic assessments, oxidative stress analysis, mitochondrial dynamics evaluation, and gene/protein expression profiling. We also provide experimental design, data analysis, and consultation services.

How do I select the right model for my research?

Our team will work closely with you to understand your research objectives and recommend the most suitable models for your study. We consider your specific needs, whether you are focusing on disease mechanisms, therapeutic efficacy, or the effects of environmental factors.

Can you customize models for my research?

Yes! We specialize in developing customized models tailored to your research needs. Whether you need to simulate specific mitochondrial dysfunctions, assess drug effects, or model genetic mutations, we can design a model to meet your requirements.

What makes your models different from others?

Our models closely mimic human mitochondrial biology, providing highly relevant and reproducible results. We use state-of-the-art technology to measure mitochondrial health, allowing for comprehensive insights into mitochondrial function and dysfunction.

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Published Data

Fig.2 Diagram showing the mitochondrial dysfunction during aging. (OA Literature) Fig. 2 Mitochondrial dysfunction during aging. ²

Mitochondria are essential for energy production through oxidative phosphorylation (OXPHOS), a process that naturally generates reactive oxygen species (ROS). Under normal conditions, ROS play a role in cellular signaling and regulation. However, the body maintains a delicate balance by using antioxidant systems to control ROS levels and prevent oxidative damage. As organisms age, mitochondrial function declines due to reduced mitochondrial biogenesis, increased ROS production, and diminished capacity to manage oxidative stress. This leads to the accumulation of dysfunctional mitochondria, which exacerbates the generation of ROS. The elevated ROS levels further damage mitochondrial membranes, proteins, and DNA, creating a vicious cycle that impairs cellular function. As a result, this oxidative damage contributes to a decline in tissue function, impaired regenerative capacity, and eventually triggers apoptosis or programmed cell death. The accumulation of damaged mitochondria and the persistent oxidative stress are key contributors to aging-related diseases, including neurodegeneration, cardiovascular disorders, and muscle weakness. Understanding how mitochondrial dysfunction and ROS production accelerate aging can provide valuable insights for developing therapeutic strategies to mitigate age-related cellular damage.

References

Martic, Ines et al. "Mitochondrial dynamics and metabolism across skin cells: implications for skin homeostasis and aging." Frontiers in physiology vol. 14 1284410. 15 Nov. 2023, DOI:10.3389/fphys.2023.1284410. Distributed under Open Access license CC BY 4.0, without modification.
Strickland, Marie et al. "Relationships Between Ion Channels, Mitochondrial Functions and Inflammation in Human Aging." Frontiers in physiology vol. 10 158. 1 Mar. 2019, DOI:10.3389/fphys.2019.00158. Distributed under Open Access license CC BY 4.0, without modification.