Journal of Clinical Endocrinology Research

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Editorial - Journal of Clinical Endocrinology Research (2023) Volume 6, Issue 4

Mitochondrial energetics in neurodegenerative diseases: Insights and therapeutic avenues

Subramanya Srikantan *

Department of Medicine, Center for Precision Medicine, San Antonio, USA

Corresponding Author:
Subramanya Srikantan
Department of Medicine
University of Texas Health San Antonio, San Antonio, USA.
E-mail:
subramany02r@uthscsa.edu

Received: 10-Jul-2023, Manuscript No. AAJCER-23-113393; Editor assigned: 12-Jul-2023, PreQC No. AAJCER-23-113393(PQ); Reviewed: 26-Jul-2023, QC No. AAJCER-23-113393; Revised: 28-Jul-2023, Manuscript No. AAJCER-23-113393(R); Published: 04-Aug-2023, DOI:10.35841/aajcer-6.4.158

Citation: Srikantan S. Mitochondrial energetics in neurodegenerative diseases: Insights and therapeutic avenues. J Clin Endocrinol Res. 2023;6(4):158

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Mitochondria, the cellular powerhouses, are emerging as pivotal players in drug development. Researchers are exploring how understanding and manipulating mitochondrial energetics can lead to the development of innovative and targeted therapies for a wide range of diseases, from cancer to neurodegenerative disorders [1].

. This topic investigates the promising intersection of mitochondrial biology and drug discovery, offering potential breakthroughs in medical treatments.

 

 

Neurodegenerative diseases, a group of disorders characterized by the progressive degeneration of neurons, present a formidable challenge in the field of medicine. Conditions like Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Huntington's disease inflict considerable suffering on patients and their families. While the exact causes of these diseases remain complex and multifaceted, recent research has shed light on a common denominator in their pathology: mitochondrial dysfunction and disrupted mitochondrial energetics [2].

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Mitochondria, often referred to as the "powerhouses of the cell," are double-membraned organelles responsible for generating adenosine triphosphate (ATP), the cell's primary energy currency. Mitochondrial energetics, or the processes that govern energy production within these tiny structures, play a pivotal role in neuronal health and function. Studies have increasingly shown that mitochondrial dysfunction is a recurring theme in neurodegenerative diseases. Here are some key insights into this connection: In neurodegenerative diseases, mitochondrial energetics are often compromised, leading to energy deficits in neurons. As neurons are particularly energy-demanding cells, this shortfall can disrupt their normal functioning and contribute to disease progression.

 

Dysfunctional mitochondria can produce excessive reactive oxygen species (ROS), leading to oxidative stress [3].

. This oxidative damage can harm cellular components, including proteins, lipids, and DNA, exacerbating the neurodegenerative process.Mitochondria play a crucial role in regulating intracellular calcium levels. Dysfunctional mitochondria can lead to calcium dysregulation, which can trigger neuronal cell death.Mitochondrial DNA Mutations: Some neurodegenerative diseases are associated with mutations in mitochondrial DNA, further implicating mitochondrial dysfunction in disease pathogenesis. Understanding the link between mitochondrial energetics and neurodegenerative diseases has opened up new avenues for potential treatments:

 

 

Researchers are exploring drugs and compounds that specifically target and improve mitochondrial function. These therapies aim to enhance ATP production and reduce oxidative stress. Physical activity and certain diets have shown promise in supporting mitochondrial health. Lifestyle interventions that promote mitochondrial biogenesis and function may offer protective effects against neurodegeneration. Antioxidants, which counteract oxidative stress, are being investigated for their potential to mitigate mitochondrial damage in neurodegenerative diseases [4].

. Advances in gene editing technologies offer the potential to correct or replace mutated mitochondrial DNA, potentially slowing or halting disease progression.

 

 

Mitochondria, the cellular powerhouses, are multi-talented organelles that play a pivotal role in various aspects of cellular function. From respiratory processes and energy production to intracellular signaling, mitochondria are indispensable for the smooth operation of a cell's intricate machinery. These dynamic organelles are highly responsive to environmental factors, adjusting their morphology, number, and function in response to changing conditions, including hormonal cues, dietary shifts, temperature variations, and even exercise.

 

However, their significance extends far beyond the cellular realm. Mitochondria are key players in the balance between life and death within a cell. They wield a remarkable influence over cell survival and apoptosis, making them central figures in the aging process. Their impact is particularly pronounced in the Central Nervous System (CNS), where neuronal survival and excitability rely heavily on a consistent and adequate supply of energy from mitochondrial sources. Consequently, any disruption in mitochondrial function can have profound consequences, rendering the brain exceptionally vulnerable to dysfunction. Maintaining the health and functionality of mitochondria is not merely a cellular luxury; it's a fundamental necessity. Proper mitochondrial function is essential for initiating stress responses and upholding metabolic equilibrium. These processes, in turn, have been implicated not only in extending lifespan but also in shaping the aging process itself [5].

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To ensure the continued well-being of the cell, intricate cellular programs are at work, diligently monitoring and, when necessary, replacing dysfunctional mitochondria with new, fully operational organelles. This meticulous maintenance of mitochondrial quality and integrity serves as a vital defense mechanism, safeguarding the cell against the ravages of time and the challenges of a dynamic environment. In summary, mitochondria are the unsung heroes of cellular life, orchestrating a symphony of essential functions that impact not only individual cells but also the entire organism. Understanding their roles and vulnerabilities is paramount, as it opens doors to interventions that may combat aging, protect against neurodegeneration, and promote overall health and longevity

Conclusion

Whole-Body Electromyostimulation is a game-changing fitness technology with the potential to transform the way we exercise. By harnessing the power of electrical impulses to engage muscles effectively, it offers a host of benefits, including accelerated muscle growth, fat loss, time efficiency, reduced injury risk, improved athletic performance, and convenience. While WB-EMS is a promising innovation, it's essential to approach it with a balanced perspective. As with any fitness regimen, it should be integrated into a holistic wellness plan that includes proper nutrition, adequate rest, and other essential components of a healthy lifestyle. Additionally, individuals with certain medical conditions or those who are pregnant should consult with a healthcare professional before incorporating WB-EMS into their fitness routine. As the fitness industry continues to evolve, Whole-Body Electromyostimulation stands out as a remarkable tool that can help individuals achieve their fitness goals efficiently, making it an electrifying addition to the world of workouts.

References

  1. Wu ZD, Huang XM, Feng YJ, et al. Transducer of regulated CREB?binding proteins (TORCs) induce PGC?1 alpha transcription and mitochondrial biogenesis in muscle cells. Proc Natl Acad Sci USA. 2006;103:14379–14384.
  2. Indexed at, Google Scholar, Cross Ref

  3. Scarpulla RC. Metabolic control of mitochondrial biogenesis through the PGC?1 family regulatory network. Biochim Biophys Acta. 2011;1813:1269–1278.
  4. Indexed at, Google Scholar, Cross Ref

  5. Yin W, Signore AP, Iwai M, et al. Rapidly increased neuronal mitochondrial biogenesis after hypoxic?ischemic brain injury. Stroke. 2008;39:3057–3063. 4.
  6. Indexed at, Google Scholar, Cross Ref

  7. Chen YC, Wu JS, Tsai HD, et al. Peroxisome proliferator?activated receptor gamma (PPAR?gamma) and neurodegenerative disorders. Mol Neurobiol. 2012;46:114–124.
  8. Indexed at, Google Scholar, Cross Ref

  9. Canto C, Gerhart?Hines Z, Feige JN, et al. AMPK regulates energy expenditure by modulating NAD(+) metabolism and SIRT1 activity. Nat. 2009;458:1056–140.
  10. Indexed at, Google Scholar, Cross Ref

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