Short Communication, J Biochem Physiol Vol: 6 Issue: 3
Mitochondrial Dysfunction in Age-Related Physiological Decline and Disease
Richard Lino*
1Department of Biochemistry Section, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, USA
*Corresponding Author: Richard Lino,
Department of Biochemistry Section,
National Institute of Neurological Disorders and Stroke, NIH, Bethesda, USA
E-mail: linoricharg@nds.edu
Received date: 22 August, 2023, Manuscript No. JBPY-23-117706;
Editor assigned date: 24 August, 2023, Pre QC No. JBPY-23-117706 (PQ);
Reviewed date: 13 September, 2023, QC No. JBPY-23-117706;
Revised date: 21 September, 2023, Manuscript No: JBPY-23-117706 (R);
Published date: 28 September, 2023, DOI: 10. 4172/jbpy.1000146
Citation: Lino R (2023) Mitochondrial Dysfunction in Age-Related Physiological Decline and Disease. J Biochem Physiol 6:3.
Description
The mitochondria often referred to as the "powerhouses of the cell," play a central role in energy production and various metabolic processes within our bodies. However, as we age, these vital organelles can experience dysfunction, leading to a range of agerelated physiological changes and contributing to the development of several diseases.
Mitochondria are double-membraned organelles found in the cells of most living organisms. They are responsible for generating Adenosine Triphosphate (ATP), which serves as the primary energy currency for cells. In addition to energy production, mitochondria are involved in processes like cell signaling, cellular differentiation, and the regulation of the cell cycle [1-3].
Mitochondrial dysfunction and aging
The process of aging is characterized by a gradual decline in physiological function, often accompanied by an increased susceptibility to diseases. Mitochondrial dysfunction is a significant contributor to this decline. There are several mechanisms by which mitochondrial dysfunction can affect the aging process:
Energy production: As mitochondria are primarily responsible for energy production, any decline in their function can lead to reduced energy output. This can manifest as fatigue, reduced physical performance, and decreased metabolic efficiency [4].
Reactive Oxygen Species (ROS) production: Mitochondria are also a source of reactive oxygen species, which are chemically reactive molecules that can cause cellular damage. Increased ROS production due to mitochondrial dysfunction can lead to oxidative stress and cellular damage.
Mitochondrial DNA mutations: Mitochondria have their own DNA, separate from nuclear DNA. Over time, mutations can accumulate in mitochondrial DNA, which can lead to impaired mitochondrial function. This further exacerbates the decline in energy production and overall cellular function [5].
Impaired mitophagy: Mitophagy is the process of removing damaged or dysfunctional mitochondria. With aging, this process can become less efficient, allowing dysfunctional mitochondria to accumulate within cells [6].
Mitochondrial dysfunction and disease
The consequences of mitochondrial dysfunction extend beyond the aging process, as it is associated with the development of various diseases. Some of the most notable diseases linked to mitochondrial dysfunction include:
Neurodegenerative diseases: Mitochondrial dysfunction is strongly associated with neurodegenerative conditions such as Alzheimer's and Parkinson's disease. In these disorders, the impaired energy production and accumulation of damaged mitochondria can contribute to the death of brain cells [7].
Cardiovascular diseases: Heart muscles are particularly rich in mitochondria, making them vulnerable to dysfunction. This can lead to conditions such as heart failure and cardiomyopathies.
Metabolic disorders: Mitochondrial dysfunction can result in metabolic diseases, including type 2 diabetes. Reduced energy production can affect the body's ability to regulate blood sugar levels.
Muscle disorders: Conditions like mitochondrial myopathies, characterized by muscle weakness and pain, are directly linked to mitochondrial dysfunction [8].
Cancer: Some cancer cells display dysfunctional mitochondria, and the Warburg effect, where cancer cells favor glycolysis over oxidative phosphorylation for energy production, is well-documented.
Mitochondrial-targeted therapies
Understanding the role of mitochondrial dysfunction in aging and disease has led to the exploration of targeted therapies. Researchers are investigating various strategies to combat mitochondrial dysfunction and its associated consequences. These strategies include:
Antioxidants: Antioxidants can help mitigate the harmful effects of increased ROS production by dysfunctional mitochondria. Supplements like coenzyme Q10 and vitamins C and E have been studied for their potential in reducing oxidative stress [9,10].
Mitochondrial biogenesis: Stimulating the creation of new, healthy mitochondria is another approach. Exercise and caloric restriction have been shown to support mitochondrial biogenesis.
Pharmaceutical interventions: Various drugs are being studied to address mitochondrial dysfunction. These include compounds that can boost mitochondrial function or stimulate mitophagy to remove damaged mitochondria.
Gene therapies: Gene therapy approaches aim to replace or repair mutated mitochondrial DNA to restore proper function.
Mitochondrial dysfunction is a critical factor in age-related physiological decline and the development of numerous diseases. It affects energy production, contributes to oxidative stress, and leads to the accumulation of damaged mitochondria. As our understanding of these processes deepens, so does our ability to develop interventions and therapies to mitigate the impact of mitochondrial dysfunction. Ultimately, this research holds promise for extending healthy lifespan and reducing the burden of age-related diseases.
References
- Soudais C, de Villartay JP, Le Deist F, Fischer A, Lisowska-Grospierre B(1993) Independent mutations of the human CD3–ε gene resulting in a T cell receptor/CD3 complex immunodeficiency. Nat Genet 3(1):77-81.
- Blumberg RS, Ley S, Sancho J, Lonberg N, Lacy E, et al. (1990) Structure of the T-cell antigen receptor: Evidence for two CD3 epsilon subunits in the T-cell receptor-CD3 complex. Proc Natl Acad Sci 87(18):7220-7224.
- Sun N, Youle RJ, Finkel T (2016) The mitochondrial basis of aging. Mol Cell 61:654–666.
[CrossRef] [Google Scholar] [PubMed]
- Wallace DC (2012) Mitochondria and cancer. Nat Rev Cancer 12:685–698.
[CrossRef] [Google Scholar] [PubMed]
- Linnane AW, Marzuki S, Ozawa T, Tanaka M (1989) Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases. Lancet 1:642–645.
[PubMed] [CrossRef] [Google Scholar]
- Muller-Hocker J (1998) Cytochrome-c-oxidase deficient cardiomyocytes in the human heart—An age-related phenomenon. A histochemical ultracytochemical study. Am J Pathol. 1989;134:1167–1173.
[PubMed] [Google Scholar]
- Itoh K, Weis S, Mehraein P, Muller-Hocker J (1996) Cytochrome c oxidase defects of the human substantia nigra in normal aging. Neurobiol. Aging 17:843–848.
[CrossRef] [Google Scholar] [PubMed]
- Khrapko K, Kraytsberg Y, Grey AD, Vijg J, Schon EA (2006) Does premature aging of the mtDNA mutator mouse prove that mtDNA mutations are involved in natural aging? Aging Cell 5:279–282.
[CrossRef] [Google Scholar] [PubMed]
- Balaban RS, Nemoto S, Finkel T (2005) Mitochondria, oxidants, and aging. Cell 120:483–495.
[CrossRef] [Google Scholar] [PubMed]
- Edgar D, Shabalina I, Camara Y, Wredenberg A, Calvaruso MA, et al. (2009) Random point mutations with major effects on protein-coding genes are the driving force behind premature aging in mtDNA mutator mice. Cell Metab 10:131–138.
[CrossRef] [Google Scholar] [PubMed]
