Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Obesity is a chronic metabolic disorder and a growing global public health challenge, affecting hundreds of millions of individuals worldwide. While diet and physical activity are well-established contributors, increasing evidence underscores the critical role of epigenetic mechanisms in mediating obesity-related processes. Epigenetic modifications-such as DNA methylation, RNA methylation (particularly N6-methyladenosine), histone modifications, non-coding RNAs, and chromatin remodeling-modulate gene expression without altering the DNA sequence. This review aims to provide an overview of the epigenetic mechanisms involved in obesity, with an emphasis on their molecular functions and regulatory networks. Integrating findings from relevant studies, we discuss how these modifications influence obesity-related outcomes through regulating key processes such as adipocyte differentiation and energy metabolism. Advancing our understanding of epigenetic regulation may pave the way for novel, targeted strategies in the prevention and treatment of obesity.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12293253PMC
http://dx.doi.org/10.3390/cimb47070540DOI Listing

Publication Analysis

Top Keywords

epigenetic regulation
8
epigenetic mechanisms
8
epigenetic
5
dynamic rendition
4
rendition adipose
4
adipose genes
4
genes epigenetic
4
regulation revealing
4
revealing mechanisms
4
obesity
4

Similar Publications

Human cord blood (CB) myeloid progenitor reprogramming to a high-fidelity human induced pluripotent stem cell (hiPSC) state can be achieved using non-integrating episomal vectors and stromal signals. These conventional, primed CB-hiPSC lines can subsequently be chemically reverted with high efficiencies to a blastomere-like Tankyrase/PARP Inhibitor-Regulated Naive Stem Cell (TIRN-SC) state with functional totipotency. PARP-regulated TIRN-SCs are human stem cells with high epigenetic plasticity, stable epigenomic imprints, and have greater differentiation potency than conventional, lineage-primed hiPSCs.

View Article and Find Full Text PDF

Multiple myeloma (MM) continues to be an incurable malignancy, even with recent therapeutic advancements. While epigenetic dysregulation at cis-regulatory elements is known to drive disease progression, the complete molecular mechanisms underlying these alterations are poorly understood. Using ATAC-seq analysis combined with computational footprinting of CD138+ cells from 55 MM patients, we depicted the dynamic changes in chromatin accessibility during disease progression and identified Nuclear Respiratory Factor 1 (NRF1) as a master regulator of vital MM survival pathways.

View Article and Find Full Text PDF

Hypoxia Aggravates Myocardial Ischemia/Reperfusion Injury Through the Promotion of Ferroptosis via ACSL4 Lactylation.

J Cardiovasc Transl Res

September 2025

Department of Cardiology, Bei'an Hospital, Beidahuang Group, Heihe, 164000, Heilongjiang Province, China.

Myocardial ischemia/reperfusion injury (MIRI) worsens ischemic damage, with ferroptosis as a key mediator of this iron-dependent cell death. Lactylation, a novel epigenetic modification, remains poorly understood in MIRI-associated ferroptosis. This study aimed to elucidate the mechanistic link between lactylation and ferroptosis in MIRI.

View Article and Find Full Text PDF

Aurora kinase A promotes trained immunity via regulation of endogenous S-adenosylmethionine metabolism.

Elife

September 2025

State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.

Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying the regulation of trained immunity remains largely elusive. Here, we demonstrate that inhibition of Aurora kinase A (AurA) dampens trained immunity induced by β-glucan. ATAC-seq and RNA-seq analysis reveal that AurA inhibition restricts chromatin accessibility of genes associated with inflammatory pathways such as JAK-STAT, TNF, and NF-κB pathways.

View Article and Find Full Text PDF

Chronic liver disease (CLD) is a leading cause of global morbidity and mortality, necessitating effective preventive strategies. Growing evidence is linking coffee consumption with reduced risk of disease progression in various CLDs, including metabolic dysfunction associated steatotic liver disease (MASLD), alcoholic liver disease, hepatitis B and C, autoimmune hepatitis, and a reduction in the risk of hepatocellular carcinoma development. Coffee, a globally consumed beverage, contains bioactive compounds like caffeine, chlorogenic acids, diterpenes, and polyphenols, which may offer hepatoprotective benefits through anti-inflammatory, antioxidant, and metabolic regulatory effects.

View Article and Find Full Text PDF