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Cell Membrane Theory of Senescence” and the Role of Bioactive Lipids in Aging, and Aging Associated Diseases and Their Therapeutic Implications

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Cell Membrane Theory of Senescence” and the Role of Bioactive Lipids in Aging, and Aging Associated Diseases and Their Therapeutic Implications biomolecules Review “Cell Membrane Theory of Senescence” and the Role of Bioactive Lipids in Aging, and Aging Associated Diseases and Their Therapeutic Implications Undurti N. Das 1,2,3 1 UND Life Sciences, 2221 NW 5th St, Battle Ground, WA 98604, USA; [email protected]; Tel.: +508-904-5376 2 BioScience Research Centre and Department of Medicine, GVP Medical College and Hospital, Visakhapatnam 530048, India 3 International Research Centre, Biotechnologies of the third Millennium, ITMO University, 191002 Saint-Petersburg, Russia Abstract: Lipids are an essential constituent of the cell membrane of which polyunsaturated fatty acids (PUFAs) are the most important component. Activation of phospholipase A2 (PLA2) induces the release of PUFAs from the cell membrane that form precursors to both pro- and ant-inflammatory bioactive lipids that participate in several cellular processes. PUFAs GLA (gamma-linolenic acid), DGLA (dihomo-GLA), AA (arachidonic acid), EPA (eicosapentaenoic acid) and DHA (docosahex- aenoic acid) are derived from dietary linoleic acid (LA) and alpha-linolenic acid (ALA) by the action of desaturases whose activity declines with age. Consequently, aged cells are deficient in GLA, DGLA, AA, AA, EPA and DHA and their metabolites. LA, ALA, AA, EPA and DHA can also be obtained direct from diet and their deficiency (fatty acids) may indicate malnutrition and deficiency of several minerals, trace elements and vitamins some of which are also much needed co-factors Citation: Das, U.N. “Cell Membrane for the normal activity of desaturases. In many instances (patients) the plasma and tissue levels of Theory of Senescence” and the Role GLA, DGLA, AA, EPA and DHA are low (as seen in patients with hypertension, type 2 diabetes of Bioactive Lipids in Aging, and mellitus) but they do not have deficiency of other nutrients. Hence, it is reasonable to consider that Aging Associated Diseases and Their the deficiency of GLA, DGLA, AA, EPA and DHA noted in these conditions are due to the decreased Therapeutic Implications. activity of desaturases and elongases. PUFAs stimulate SIRT1 through protein kinase A-dependent Biomolecules 2021, 11, 241. https:// α doi.org/10.3390/biom11020241 activation of SIRT1-PGC1 complex and thus, increase rates of fatty acid oxidation and prevent lipid dysregulation associated with aging. SIRT1 activation prevents aging. Of all the SIRTs, SIRT6 is Academic Editors: Rosario critical for intermediary metabolism and genomic stability. SIRT6-deficient mice show shortened Francesco Donato and Mario Ollero lifespan, defects in DNA repair and have a high incidence of cancer due to oncogene activation. SIRT6 Received: 23 November 2020 overexpression lowers LDL and triglyceride level, improves glucose tolerance, and increases lifespan Accepted: 1 February 2021 of mice in addition to its anti-inflammatory effects at the transcriptional level. PUFAs and their Published: 8 February 2021 anti-inflammatory metabolites influence the activity of SIRT6 and other SIRTs and thus, bring about their actions on metabolism, inflammation, and genome maintenance. GLA, DGLA, AA, EPA and Publisher’s Note: MDPI stays neutral DHA and prostaglandin E2 (PGE2), lipoxin A4 (LXA4) (pro- and anti-inflammatory metabolites of with regard to jurisdictional claims in AA respectively) activate/suppress various SIRTs (SIRt1 SIRT2, SIRT3, SIRT4, SIRT5, SIRT6), PPAR-γ, published maps and institutional affil- PARP, p53, SREBP1, intracellular cAMP content, PKA activity and peroxisome proliferator-activated iations. receptor γ coactivator 1-α (PGC1-α). This implies that changes in the metabolism of bioactive lipids as a result of altered activities of desaturases, COX-2 and 5-, 12-, 15-LOX (cyclo-oxygenase and lipoxygenases respectively) may have a critical role in determining cell age and development of several aging associated diseases and genomic stability and gene and oncogene activation. Thus, Copyright: © 2021 by the author. methods designed to maintain homeostasis of bioactive lipids (GLA, DGLA, AA, EPA, DHA, PGE2, Licensee MDPI, Basel, Switzerland. LXA4) may arrest aging process and associated metabolic abnormalities. This article is an open access article distributed under the terms and Keywords: aging; unsaturated fatty acids; bioactive lipids; inflammation; cell membrane; sirtuins conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). Biomolecules 2021, 11, 241. https://doi.org/10.3390/biom11020241 https://www.mdpi.com/journal/biomolecules Biomolecules 2021, 11, 241 2 of 40 1. Introduction Aging is inevitable. It is associated with time-dependent decline in physical activity Biomolecules 2021, 11, x FOR PEER REVIEWand physiological function, and slow but steady decrease in organ function that even- tually leads to death. With increasing age, aging associated diseases occur that include insulin resistance, type 2 diabetes mellitus, hypertension, hyperlipidemia or dyslipidemia, 1.coronary Introduction heart disease, Alzheimer’s disease, and cancer. Aging induces perceptible and time-dependentAging is inevitable. changes It is associated in the with immune time-dependent system decline and gradual in physical increase activity in plasma inflam- andmatory physiological markers function, interleukin-6 and slow but (IL-6) steady and decrease tumor in organ necrosis function factor- that αeventu-(TNF-α) with a parallel allydecrease leads to indeath. anti-inflammatory With increasing age, cytokines aging associated IL-4 and diseases IL-10. occur However, that include it isin- not known whether sulin resistance, type 2 diabetes mellitus, hypertension, hyperlipidemia or dyslipidemia, coronarychanges heart in thedisease, levels Alzheimer’s of cytokines disease, are and inevitable cancer. Aging with induces aging perceptible or are a signal and of the impending timeaging-dependent process changes or just in the a marker immune ofsystem aging. and It gradual is not increase clear whether in plasma changesinflam- in cytokines and matoryassociated markers events interleukin such-6 (IL as-6) free and radicaltumor necrosis generation factor-α (reactive(TNF-α) with oxygen a parallel species, nitric oxide, decreasecarbon in monoxide,anti-inflammatory hydrogen cytokines sulfide) IL-4 and andIL-10. antioxidants However, it is not are known as a whether result of aging. However, changes in the levels of cytokines are inevitable with aging or are a signal of the impend- ingwhat aging is process certain or isjust that a marker these ofbiochemical aging. It is not andclear whether immunological changes in changescytokines can be postponed andor associated delayed events by regular such as exercisefree radical and generation diet control (reactive (especially oxygen species, calorie nitric oxide, restriction and intermit- carbontent fasting).monoxide, Goodhydrogen dietary sulfide) practices and antioxidants and regular are as a result exercise of aging. can However, delay the development of whataging is certain associated is that these diseases biochemical obesity, and insulin immunological resistance, changes type can 2 be diabetes postponed mellitus, or hypertension, delayedmetabolic by regular syndrome, exercise and coronary diet control heart (especially disease calorie and re cancer.striction and intermittent fasting). Good dietary practices and regular exercise can delay the development of aging associatedUnderstanding diseases obesity, the insulin molecular resistance, events type 2 diabetes responsible mellitus, for hypertension, aging process met- may help to develop abolicstrategies syndrome, to slow coronary aging. heart Optimal disease and cell canc responseer. to both internal and external stimuli depends onUnderstanding the cell membrane the molecular integrity. events responsible This is so for since; aging allprocess stimuli may help need to tode- be conveyed to the velopgenome strategies through to slow the aging. cell Optimal membrane. cell response Similarly, to both all internal the responses and external elicited stimuli by the cell genome depends on the cell membrane integrity. This is so since; all stimuli need to be conveyed toneed the genome to be through conveyed the cell to membrane. the cell externalSimilarly, all milieu the responses through elicited the by cell the membrane. cell Thus, cell genomemembrane need to structurebe conveyed and to the consequently cell external milieu its functions through the are cell crucial membrane. to receiveThus, and send signals cellto membrane the external structure environment. and consequently Since its aging functions is a universalare crucial to process receive (fromand send single cell organisms signalsto humans), to the external it is possible environment. that Since understanding aging is a universal the molecular process (from events single of cell this process may have organismsimplications to humans), for all. it is Somepossible of that the understanding outlined biological the molecular mechanisms events of this ofpro- the aging proposed cess may have implications for all. Some of the outlined biological mechanisms of the ag- ingare proposed given are in given Figure in 1Figure. Thus, 1. Thus, methods methods or or strategiesstrategies developed developed to act toon actthese on these processes processesmay lead may to lead certain to certain common common management management strategies strategies of diseases of diseases associated associated with with aging and agingeventually and eventually ensure ensure delaying delaying or or
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