Commentary - (2022) Volume 8, Issue 8
Received: 01-Aug-2022, Manuscript No. IPJCE-22-14434; Editor assigned: 03-Aug-2022, Pre QC No. IPJCE-22-14434(PQ); Reviewed: 17-Aug-2022, QC No. IPJCE-22-14434; Revised: 22-Aug-2022, Manuscript No. IPJCE-22-14434(R); Published: 29-Aug-2022, DOI: 10.21767/2472-1158.8.8.37
Aging represents the multifactorial decline of physiological functions in all organisms. Several hallmarks of aging have been defined in recent decades, including epigenetic deregulation. Indeed, some epigenetic events have been found to change between different species during aging. Epigenetic changes that directly contribute to aging and age-related diseases include the accumulation of histone variants, altered chromatin accessibility, histone and heterochromatin loss, aberrant histone modifications, miRNA expression includes activity deregulation. As a result, cellular processes are affected, leading to the development or progression of several human pathologies such as cancer, diabetes, osteoporosis and neurodegenerative diseases. In this review, we focus on the epigenetic mechanisms underlying age-related processes in various species and discuss how these deregulations contribute to human disease.
About 2 billion adults worldwide are overweight, and more than half of them are classified as obese. And almost one-third of the world’s children suffer from stunting. Given the tremendous insight gained from decades of research on growth and development, why the world is in the midst of a global obesity epidemic with a double burden of malnutrition, many questions remain: Were obesity coexists with underweight and micronutrient deficiencies. This challenge to the human condition may result from nutritional and environmental stresses during pregnancy, which may program the fetus to an increased risk of chronic disease in adulthood. To explore this concept, often referred to as developmental origin, this review will focus on prenatal or childhood predisposition to obesity, fatty liver disease, hypertension, and/or type 2 diabetes (T2D). To that end, this review article examines the epidemiology of, with a focus on key environmental influences that contribute to human energy adaptation, placental development, metabolic abnormalities, and the promotion of chronic disease in adulthood. These areas complement and add to our understanding of how providing the best conditions for optimal growth can create the best conditions for lifelong health, understanding the physiological, epigenetic and molecular mechanisms of DOHaD is essential to address the global problem of obesity and other chronic diseases as comprehensively as possible.
Obesity is characterized as a complex, multifactorial excess of adipose tissue (AT) with altered immune responses and affects almost all age and socioeconomic groups worldwide. Aberrant accumulation of AT leads to several metabolic diseases, including nonalcoholic fatty liver disease (NAFLD), mild inflammation, type 2 diabetes (T2DM), Cardiovascular Disease (CVD), and cancer. AT is an endocrine organ composed of adipocytes and immune cells such as B cells, T cells and macrophages. These immune cells secrete various cytokines and chemokines and communicate with adipokines to maintain metabolic homeostasis and low-grade chronic inflammation. Novel forms of adipokines, microRNAs (miRs), are expressed in many developing peripheral tissues, including ATs, T cells, and macrophages, and regulate immune responses. MiRs are essential for insulin resistance, maintenance of the tumor microenvironment, and Obesity- Associated Inflammation (OAI). Aberrant regulation of AT, T cell, and macrophage miRs can alter the function of various organs, including pancreas, heart, liver, and skeletal muscle. Dysregulated expression of miRs in inflammatory adipocytes, T cells, and macrophages suggests the importance of miRs in OAI, as obesity and inflammation are closely linked. Therefore, in this review article, miRs as epigenetic regulators affecting adipocyte differentiation, immune response, AT browning, adipogenesis, lipid metabolism, insulin resistance (IR), glucose homeostasis, obesity, and metabolic disorders outlined the role of in addition, we describe a number of engineered miRs as novel biomarkers of metabolic disease progression and therapeutic targets in obesity.
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The authors declare that they have no conflict of interest.
Citation: Baudouin F (2022) The Immune Cells Communicate and Maintained Homeostasis in Low Grade Chronic Inflammation. J Clin Epigen. 8:37.
Copyright: © 2022 Baudouin F. 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.
