title: Are microRNAs true sensors of ageing and cellular senescence?
abstract: All living beings are programmed to death due to aging and age-related processes. Aging is a normal process of every living species. While all cells are inevitably progressing towards death, many disease processes accelerate the aging process, leading to senescence. Pathologies such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, cardiovascular disease, cancer, and skin diseases have been associated with deregulated aging. Healthy aging can delay onset of all age-related diseases. Genetics and epigenetics are reported to play large roles in accelerating and/or delaying the onset of age-related diseases. Cellular mechanisms of aging and age-related diseases are not completely understood. However, recent molecular biology discoveries have revealed that microRNAs (miRNAs) are potential sensors of aging and cellular senescence. Due to miRNAs capability to bind to the 3' untranslated region (UTR) of mRNA of specific genes, miRNAs can prevent the translation of specific genes. The purpose of our article is to highlight recent advancements in miRNAs and their involvement in cellular changes in aging and senescence. Our article discusses the current understanding of cellular senescence, its interplay with miRNAs regulation, and how they both contribute to disease processes.
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Justin
authors.initials: J
authors.lastname: Williams
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Flint
authors.initials: F
authors.lastname: Smith
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Subodh
authors.initials: S
authors.lastname: Kumar
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Murali
authors.initials: M
authors.lastname: Vijayan
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Cell Biology & Biochemistry, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neuroscience & Pharmacology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Speech, Language and Hearing Sciences Departments, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, MS 7495, Lubbock, TX 79413, United States. Electronic address: hemachandra.reddy@ttuhsc.edu.
authors.forename: P Hemachandra
authors.initials: PH
authors.lastname: Reddy
mesh_terms: D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D016922:Cellular Senescence / Q000502:physiology*; D044127:Epigenesis, Genetic; D006801:Humans; D035683:MicroRNAs / Q000096:biosynthesis / Q000378:metabolism
chemical_list: D035683:MicroRNAs
keywords: Aging; Alzheimer’s disease; Oxidative-stress; Senescence; microRNA