GET THE APP

Mitochondria: Ancient Travelers Shaping Human Health and Disease
..

Journal of Phylogenetics & Evolutionary Biology

ISSN: 2329-9002

Open Access

Commentary - (2024) Volume 12, Issue 1

Mitochondria: Ancient Travelers Shaping Human Health and Disease

Timothy Moyes*
*Correspondence: Timothy Moyes, Department of Biology, University of Brigham Young, 401 WIDB, Provo, UT 84602-5253, USA, Email:
Department of Biology, University of Brigham Young, 401 WIDB, Provo, UT 84602-5253, USA

Received: 29-Jan-2024, Manuscript No. JPGEB-24-129382; Editor assigned: 31-Jan-2024, Pre QC No. P-129382; Reviewed: 14-Feb-2024, QC No. Q-129382; Revised: 19-Feb-2024, Manuscript No. R-129382; Published: 28-Feb-2024 , DOI: 10.37421/2329-9002.2024.12.299
Citation: Moyes, Timothy. “Mitochondria: Ancient Travelers Shaping Human Health and Disease.” J Phylogenetics Evol Biol 12 (2024): 299.
Copyright: © 2024 Moyes T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Description

Mitochondria, often referred to as the powerhouse of the cell, have fascinated scientists for decades due to their unique evolutionary origin and indispensable role in cellular function. Originating from ancient bacteria that formed endosymbiotic relationships with early eukaryotic cells, mitochondria have journeyed through billions of years of evolution to become essential cellular components in all higher organisms, including humans. This article delves into the fascinating evolutionary path of mitochondria, exploring their journey from ancient bacterial immigrants to crucial players in human health and disease [1]. The origin of mitochondria can be traced back to a momentous event in the history of life on Earth known as endosymbiosis. According to the endosymbiotic theory proposed by Lynn Margulis in the 1960s, mitochondria were once free-living bacteria that were engulfed by primitive eukaryotic cells. Instead of being digested, these bacteria established a symbiotic relationship with their host cells, providing energy in the form of ATP through aerobic respiration. This mutualistic partnership was evolutionarily advantageous, leading to the integration of mitochondria into the eukaryotic cellular framework.

The integration of mitochondria into eukaryotic cells marked a pivotal moment in evolutionary history, giving rise to the complex multicellular organisms we see today. Over time, mitochondrial DNA (mtDNA) underwent significant evolutionary changes, including gene loss, gene transfer to the nuclear genome, and the acquisition of novel functions. Despite their reduced genome size compared to their bacterial ancestors, mitochondria retained essential genes encoding proteins crucial for oxidative phosphorylation and ATP production [2].

Mitochondria play a central role in cellular metabolism, acting as the primary site for ATP synthesis through oxidative phosphorylation. In addition to energy production, mitochondria are involved in various cellular processes, including calcium signaling, apoptosis, and Reactive Oxygen Species (ROS) production. Maintaining mitochondrial health is essential for overall cellular function and organismal viability. Dysfunctional mitochondria have been implicated in a wide range of human diseases, including neurodegenerative disorders, metabolic diseases, and cancer. Mitochondria are indispensable for human health, with their dysfunction contributing to the pathogenesis of numerous diseases. Inherited mitochondrial disorders, caused by mutations in either nuclear or mitochondrial genes, result in mitochondrial dysfunction and impaired energy production. These disorders often affect tissues with high energy demands, such as the brain, heart, and skeletal muscles, leading to a diverse array of clinical manifestations. Understanding the molecular mechanisms underlying mitochondrial diseases is critical for developing effective therapeutic strategies [3].

The role of mitochondria in the aging process has been a subject of intense research. The mitochondrial theory of aging proposes that cumulative damage to mitochondrial DNA and proteins over time leads to a decline in mitochondrial function and contributes to the aging phenotype. Mitochondrial dysfunction impairs cellular homeostasis, leading to the accumulation of damaged molecules and the onset of age-related diseases. Strategies aimed at improving mitochondrial function hold promise for extending healthy lifespan and delaying the onset of age-related diseases. Given their central role in cellular metabolism and disease pathogenesis, mitochondria have emerged as promising therapeutic targets for various disorders. Pharmacological interventions aimed at modulating mitochondrial function, such as antioxidants and mitochondrial biogenesis inducers, show potential for treating mitochondrial diseases and age-related conditions. Furthermore, mitochondrial transplantation and gene therapy offer innovative approaches for restoring mitochondrial function in affected tissues. As our understanding of mitochondria continues to evolve, so too does our appreciation of their significance in human health and disease. Advances in mitochondrial biology, genomics, and therapeutics hold great promise for improving the diagnosis and treatment of mitochondrial disorders and age-related conditions. Harnessing the power of mitochondria may pave the way for innovative therapies that target the root causes of disease and promote overall health and longevity [4].

Mitochondria have traveled a long evolutionary path, from ancient bacterial immigrants within eukaryotic cells to essential cellular hosts and important players in human health and disease. Their journey underscores the interconnectedness of all life forms on Earth and highlights the remarkable adaptability of biological systems. By unraveling the complexities of mitochondrial biology, we gain valuable insights into fundamental cellular processes and unlock new avenues for advancing human health and well-being [5].

Acknowledgement

Not applicable.

Conflict of Interest

There is no conflict of interest by author.

References

  1. Barreto, Felipe S., and Ronald S. Burton. "Evidence for compensatory evolution of ribosomal proteins in response to rapid divergence of mitochondrial rRNA." Mol Biol Evol 30 (2012): 310-314.
  2. Google Scholar, Crossref, Indexed at

  3. Yeaman, Sam and Michael C. Whitlock. "The genetic architecture of adaptation under migration–selection balance." Evolution 65 (2011): 1897-1911.
  4. Google Scholar, Crossref, Indexed at

  5. Blount, Zachary D., Christina Z. Borland and Richard E. Lenski. "Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli." Proc Natl Acad Sci 105 (2008): 7899-7906.
  6. Google Scholar, Crossref, Indexed at

  7. Ishikawa, Hajime. "Evolution of ribosomal RNA." Comp Biochem Physiol B 58 (1977): 1-7.
  8. Google Scholar, Crossref, Indexed at

  9. Wang, Zhong, Mark Gerstein and Michael Snyder. "RNA-Seq: A revolutionary tool for transcriptomics." Nat Rev Genet 10 (2009): 57-63.
  10. Google Scholar, Crossref, Indexed at

Google Scholar citation report
Citations: 911

Journal of Phylogenetics & Evolutionary Biology received 911 citations as per Google Scholar report

Journal of Phylogenetics & Evolutionary Biology peer review process verified at publons

Indexed In

 
arrow_upward arrow_upward