# Epigenetic Mechanisms: How Genes Are Controlled


## Key Takeaways

- Epigenetic mechanisms, including DNA methylation, histone modification, chromatin remodeling, and non-coding RNA regulation, control gene expression without altering the underlying DNA sequence, dictating cell identity and function.
- DNA methylation, primarily at CpG dinucleotides, is a stable mark often associated with gene silencing, with CpG islands in promoter regions typically remaining unmethylated to allow transcription.
- Histone modifications, such as acetylation (loosening chromatin, promoting transcription) and methylation (creating binding sites for reader proteins), form a dynamic "histone code" that influences chromatin accessibility and gene activity.
- ATP-dependent chromatin remodelers dynamically alter nucleosome positioning, sliding, or ejecting them to control access to regulatory DNA sequences, a process critical for gene regulation and often dysregulated in cancer.
- Non-coding RNAs, like miRNAs and lncRNAs (e.g., XIST), play crucial roles by post-transcriptionally regulating gene expression or by scaffolding chromatin-modifying complexes to specific genomic loci, thereby influencing epigenetic states.
- Epigenetic changes are heritable through cell division but are also reversible, a characteristic that underpins the development of epigenetic therapies targeting diseases like cancer through inhibitors of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs).

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## What Are Epigenetic Mechanisms?

### Definition and Overview

Epigenetic mechanisms are molecular processes that produce heritable changes in gene expression without altering the underlying DNA sequence. The term "epigenetics" literally means "above" or "on top of" genetics, reflecting the fact that these mechanisms act upon the genome rather than changing its primary structure. When a cell divides, epigenetic marks are copied along with the DNA, ensuring that daughter cells inherit not only the genetic code but also the instructions for which genes should be active or silent.

The four principal epigenetic mechanisms are DNA methylation, histone modification, chromatin remodeling, and regulation by non-coding RNAs. These processes work together to package the roughly two meters of DNA inside every human cell nucleus into a structure that is both compact and dynamically accessible. They determine whether a gene is tightly wound and silent or loosely packed and actively transcribed.

### The Epigenome

The complete set of epigenetic marks on a cell's genome is called the epigenome. Unlike the genome, which is largely identical across all cells of an organism, the epigenome varies dramatically between cell types. A liver cell and a neuron contain the same DNA sequence, but their epigenomes differ, which is why they express different sets of genes and perform different functions. The epigenome is also plastic—it responds to environmental signals, nutritional status, and stress, and it can be modified throughout an organism's lifetime. This plasticity is the basis for the growing interest in epigenetic therapies and the study of how lifestyle factors influence gene expression.

## DNA Methylation

### How DNA Methylation Works

DNA methylation is the covalent addition of a methyl group (—CH₃) to the fifth carbon of the cytosine base, producing 5-methylcytosine. In mammals, this reaction occurs almost exclusively at cytosine residues that are followed by guanine, known as CpG dinucleotides. The enzymes responsible are the DNA methyltransferases (DNMTs). DNMT3A and DNMT3B establish new methylation patterns during embryonic development, while DNMT1 maintains existing patterns during DNA replication by recognizing hemimethylated DNA—where one strand is methylated and the newly synthesized strand is not—and adding methyl groups to the daughter strand.

The reaction uses S-adenosylmethionine (SAM) as the methyl donor. In a typical mammalian genome, approximately 70–80% of all CpG dinucleotides are methylated. However, CpG-rich regions called CpG islands, which are often found in gene promoter regions, are usually unmethylated. These islands are typically 300–3,000 base pairs long and are present in about 60–70% of human gene promoters.

### Role in Gene Silencing

Methylation of CpG islands in promoter regions is strongly associated with transcriptional silencing. This occurs through two main mechanisms. First, methylated cytosines physically impede the binding of [transcription factors](/knowledge/molecular-biology/transcription-factor) that require unmethylated recognition sequences. Second, methylated DNA recruits methyl-CpG-binding domain (MBD) proteins, such as MeCP2 and MBD1, which in turn recruit histone deacetylases and other chromatin-modifying enzymes that compact the local chromatin structure.

DNA methylation plays critical roles in normal development. During embryogenesis, global demethylation followed by cell-type-specific remethylation establishes the distinct expression patterns of different tissues. In genomic imprinting, methylation marks one parental allele as silent, ensuring monoallelic expression of certain genes. Aberrant DNA methylation is a hallmark of cancer: [tumor suppressor genes](/knowledge/molecular-biology/tumor-suppressor-gene) are often silenced by promoter hypermethylation, while global hypomethylation can activate oncogenes and promote genomic instability. For this reason, inhibitors of DNMTs, such as 5-azacytidine and decitabine, are used clinically to treat myelodysplastic syndromes and certain leukemias.

## Histone Modifications

### Acetylation and Deacetylation

Histones are the protein components of chromatin around which DNA is wrapped. The core histones—H2A, H2B, H3, and H4—form an octamer, and approximately 147 base pairs of DNA wrap around this octamer to form a nucleosome. Each histone has an unstructured N-terminal tail that protrudes from the nucleosome and is subject to numerous post-translational modifications.

Histone acetylation is the addition of an acetyl group to lysine residues on histone tails. This reaction is catalyzed by histone acetyltransferases (HATs), such as p300 and CBP, which use acetyl-CoA as the acetyl donor. Acetylation neutralizes the positive charge of lysine, weakening the electrostatic interaction between the histone tail and the negatively charged DNA backbone. This loosens the chromatin structure, making the DNA more accessible to transcription machinery. Conversely, histone deacetylases (HDACs) remove acetyl groups, restoring the positive charge and promoting chromatin compaction and gene silencing.

The steady-state level of acetylation at any genomic locus reflects the balance between HAT and HDAC activity. For example, HDAC inhibitors such as trichostatin A and vorinostat are used in research and clinically as anti-cancer agents because they shift this balance toward acetylation, reactivating silenced tumor suppressor genes.

### Methylation and Other Marks

Histone methylation involves the addition of one, two, or three methyl groups to lysine or arginine residues. Unlike acetylation, methylation does not change the charge of the histone tail. Instead, it creates binding sites for specific reader proteins that interpret the mark. The functional outcome depends on which residue is methylated and to what degree.

Two well-characterized marks illustrate this specificity. Trimethylation of lysine 4 on histone H3 (H3K4me3) is found at active gene promoters and is associated with transcriptional activation. In contrast, trimethylation of lysine 27 on histone H3 (H3K27me3) is a hallmark of facultative heterochromatin and is deposited by the Polycomb repressive complex 2 (PRC2), leading to gene silencing. H3K9me3 marks constitutive heterochromatin, such as centromeres and telomeres, and is recognized by heterochromatin protein 1 (HP1).

Other histone modifications include phosphorylation of serine and threonine residues, which is involved in DNA damage response and chromosome condensation during mitosis; ubiquitination of lysine residues, which plays roles in both activation and silencing depending on context; and ADP-ribosylation, which contributes to DNA repair. The combinatorial pattern of these modifications is sometimes called the "histone code," though the extent to which this code is deterministic rather than probabilistic remains an active area of research.

## Chromatin Remodeling

### ATP-Dependent Remodeling

Chromatin remodeling complexes are multi-protein machines that use the energy of ATP hydrolysis to alter nucleosome positioning. These complexes belong to four main families in mammals: SWI/SNF, ISWI, CHD, and INO80. Each family contains an ATPase subunit that translocates along DNA, and the complexes can perform several distinct functions.

The primary activities of chromatin remodelers are nucleosome sliding, where the histone octamer is moved along the DNA to expose or occlude regulatory sequences; nucleosome ejection, where histones are removed entirely, creating nucleosome-free regions; and histone exchange, where canonical histones are replaced with histone variants such as H2A.Z or H3.3. For example, the SWI/SNF complex can slide or eject nucleosomes at gene promoters, while the ISWI family tends to space nucleosomes regularly, promoting chromatin compaction.

These processes are ATP-dependent and typically require concentrations of 1–5 mM ATP in the cellular environment. The energy from ATP hydrolysis is used to break histone-DNA contacts and translocate the DNA relative to the histone octamer. Mutations in SWI/SNF subunits are found in approximately 20% of human cancers, underscoring the importance of proper chromatin remodeling in maintaining normal gene expression patterns.

### Chromatin States

Chromatin exists in two broad states. Euchromatin is relatively decondensed, gene-rich, and generally transcriptionally active. Heterochromatin is compact, gene-poor, and transcriptionally silent. Heterochromatin is further divided into constitutive heterochromatin, which is permanently silent and found at centromeres and telomeres, and facultative heterochromatin, which can switch between active and silent states depending on developmental or environmental cues.

These states are not binary but exist along a continuum. A given genomic region can adopt different chromatin states in different cell types, and these states are maintained by positive feedback loops. For example, H3K9me3 recruits HP1, which in turn recruits the methyltransferase SUV39H1 that deposits more H3K9me3, creating a self-propagating silent state. Similarly, active marks recruit histone acetyltransferases and chromatin remodelers that maintain an open configuration. The interplay between chromatin remodelers and histone-modifying enzymes establishes and maintains these stable but reversible states.

## Non-Coding RNAs in Epigenetics

### MicroRNAs

MicroRNAs (miRNAs) are small, single-stranded RNA molecules of approximately 21–23 nucleotides that regulate gene expression post-transcriptionally. They are transcribed from miRNA genes, processed in the nucleus by the enzyme Drosha, and then in the cytoplasm by Dicer to produce mature miRNAs. These mature miRNAs are loaded into the RNA-induced silencing complex (RISC), where they guide the complex to complementary sequences in messenger RNA (mRNA) molecules.

The primary mechanism of miRNA action is base-pairing with the 3' untranslated region (UTR) of target mRNAs. In animals, this pairing is often imperfect, with perfect complementarity required only in the "seed region" (nucleotides 2–8) of the miRNA. This imperfect pairing leads to translational repression and mRNA destabilization through deadenylation and decapping. A single miRNA can target hundreds of different mRNAs, and it is estimated that more than 60% of human protein-coding genes are regulated by miRNAs.

While miRNAs primarily act at the mRNA level rather than at the chromatin level, they are often classified as epigenetic regulators because they create heritable changes in gene expression patterns. Some miRNAs also indirectly affect epigenetic states by targeting the mRNAs of DNMTs, HDACs, and Polycomb group proteins, creating feedback loops between different epigenetic layers.

### Long Non-Coding RNAs

Long non-coding RNAs (lncRNAs) are RNA molecules longer than 200 nucleotides that do not encode proteins. They are involved in a wide range of epigenetic processes, often acting as scaffolds that bring together chromatin-modifying complexes and guide them to specific genomic loci.

The most extensively studied example is X-inactive specific transcript (XIST), a 17-kilobase lncRNA that is expressed from the future inactive X chromosome in female mammals. XIST coats the chromosome in cis and recruits the Polycomb repressive complex PRC2, which deposits H3K27me3 marks, leading to chromosome-wide silencing. Another example is HOTAIR, a lncRNA expressed from the HOXC locus that interacts with both PRC2 and the LSD1/CoREST complex, targeting them to the HOXD locus to repress gene expression in trans.

In plants, lncRNAs and small interfering RNAs (siRNAs) direct RNA-directed DNA methylation (RdDM). In this process, 24-nucleotide siRNAs guide the DNA methyltransferase DRM2 to complementary DNA sequences, resulting in de novo methylation of cytosines in all sequence contexts. This pathway is essential for silencing [transposable elements](/knowledge/molecular-biology/transposable-element) and maintaining genome integrity in plants.

## How Epigenetic Mechanisms Are Studied

### DNA Methylation Analysis

The gold standard for detecting DNA methylation is [bisulfite sequencing](/knowledge/molecular-biology/bisulfite-sequencing). Treatment of genomic DNA with sodium bisulfite converts unmethylated cytosines to uracil, while methylated cytosines remain unchanged. After PCR amplification and sequencing, the presence of a cytosine at a CpG site indicates that it was methylated in the original sample, while a thymine (converted from uracil) indicates unmethylated DNA.

Bisulfite conversion is typically performed at 50°C for 12–16 hours in the presence of 3–5 M sodium bisulfite at pH 5.0. Whole-genome [bisulfite sequencing](/knowledge/molecular-biology/bisulfite-sequencing) (WGBS) provides single-nucleotide resolution of methylation across the entire genome but is expensive. Reduced representation bisulfite sequencing (RRBS) enriches for CpG-rich regions using restriction enzymes such as MspI, which cuts at CCGG sites, reducing cost while retaining coverage of most promoters and CpG islands. For targeted analysis, methylation-specific PCR (MSP) uses primers that discriminate between methylated and unmethylated DNA after bisulfite conversion.

### Chromatin Immunoprecipitation (ChIP)

Chromatin immunoprecipitation followed by sequencing (ChIP-seq) is the standard method for mapping histone modifications and transcription factor binding sites genome-wide. The procedure involves several steps:

1. Cross-link proteins to DNA using formaldehyde at a final concentration of 1% for 10 minutes at room temperature.
2. Quench the cross-linking reaction with glycine at a final concentration of 125 mM.
3. Lyse the cells and fragment the chromatin by sonication to produce DNA fragments of approximately 200–600 base pairs.
4. Immunoprecipitate the protein of interest using a specific antibody coupled to protein A or protein G magnetic beads.
5. Reverse the cross-links by heating at 65°C for 4–6 hours in the presence of proteinase K.
6. Purify the DNA and prepare it for high-throughput sequencing.

The resulting data reveal the genomic locations where the protein of interest was bound. ChIP-seq is widely used to map histone modifications such as H3K4me3 and H3K27me3, as well as the binding sites of transcription factors and chromatin remodelers.

### Accessibility Assays

Assays for chromatin accessibility identify regions of the genome that are open and potentially active. The assay for transposase-accessible chromatin using sequencing (ATAC-seq) has become the method of choice due to its simplicity and low input requirements. The hyperactive Tn5 transposase simultaneously fragments accessible chromatin and inserts sequencing adapters into the DNA. After PCR amplification and sequencing, regions of high read density correspond to open chromatin.

ATAC-seq requires only 50,000–100,000 cells and can be completed in a single day. The protocol involves incubating isolated nuclei with the Tn5 transposase at 37°C for 30 minutes, followed by purification and PCR amplification. The number of PCR cycles is typically 5–12, depending on the input amount. ATAC-seq data can be used to identify promoters, enhancers, and other regulatory elements, and to infer transcription factor binding through footprinting analysis.

## Examples of Epigenetic Mechanisms in Action

### X-Chromosome Inactivation

In female mammals, one of the two X chromosomes is silenced in each cell to achieve dosage compensation with males, who have a single X chromosome. This process, called X-chromosome inactivation, is initiated early in embryonic development by the XIST lncRNA. The choice of which X chromosome to inactivate is random in most tissues, meaning that female mammals are mosaics of cells expressing either the maternal or paternal X chromosome.

The inactive X chromosome is characterized by a distinct set of epigenetic marks: it is coated with XIST RNA, enriched for H3K27me3 and H3K9me2, depleted of H3K4me3 and histone acetylation, and heavily methylated at CpG islands in promoter regions. The DNA replication of the inactive X chromosome occurs late in S phase, and the chromosome adopts a compact structure visible as the Barr body. Once established, the inactive state is stably maintained through cell divisions, providing a classic example of [epigenetic inheritance](/knowledge/molecular-biology/epigenetic-inheritance) at the chromosome level.

### Genomic Imprinting

Genomic imprinting is an epigenetic phenomenon in which certain genes are expressed from only one parental allele. Approximately 100–200 imprinted genes are known in humans, and they are often clustered in genomic regions controlled by imprinting control regions (ICRs). These ICRs are differentially methylated between the maternal and paternal alleles.

The classic example is the IGF2/H19 locus on chromosome 11. The insulin-like growth factor 2 (IGF2) gene is expressed only from the paternal allele, while the adjacent H19 lncRNA is expressed only from the maternal allele. This reciprocal expression is controlled by a differentially methylated region (DMR) located between the two genes. On the paternal chromosome, the DMR is methylated, which prevents the binding of the insulator protein CTCF. This allows an enhancer downstream of H19 to activate IGF2 expression. On the maternal chromosome, the DMR is unmethylated, CTCF binds and creates an insulator that blocks the enhancer from reaching IGF2, allowing it to activate H19 instead.

Disruption of imprinting causes human diseases. Loss of methylation at the IGF2/H19 ICR leads to Beckwith-Wiedemann syndrome, characterized by overgrowth and predisposition to tumors, while gain of methylation causes Silver-Russell syndrome, characterized by growth restriction. The [Genomic Imprinting](/knowledge/molecular-biology/genomic-imprinting) mechanism illustrates how a single methylation mark can control the expression of multiple genes in a parent-of-origin-specific manner.

### Cell Differentiation

During development, pluripotent stem cells differentiate into all cell types of the body. This process involves profound changes in the epigenome. As cells commit to a particular lineage, genes required for other lineages are progressively silenced by DNA methylation and Polycomb-mediated H3K27me3, while lineage-specific genes acquire active marks such as H3K4me3 and histone acetylation.

For example, in hematopoietic stem cells differentiating into erythrocytes, the globin genes undergo a developmental switch. The embryonic and fetal globin genes are progressively silenced by DNA methylation and histone deacetylation, while the adult β-globin gene is activated by the recruitment of transcription factors and chromatin remodelers that establish an active chromatin domain. This developmental regulation is recapitulated in the [Lac Operon](/knowledge/molecular-biology/lac-operon) paradigm of inducible gene expression, though the timescale and mechanisms differ fundamentally—the lac operon responds to environmental signals within minutes, while epigenetic changes during differentiation occur over days and are maintained for the life of the cell.

## Common Pitfalls and Misconceptions

### Epigenetics vs. Mutations

A frequent confusion is equating epigenetic changes with mutations. Mutations are alterations in the DNA sequence itself—substitutions, insertions, deletions, or rearrangements. Epigenetic changes are modifications to the DNA or its associated proteins that do not change the sequence. A mutation in a gene promoter might destroy a transcription factor binding site permanently; an [epigenetic modification](/knowledge/molecular-biology/epigenetic-modification) might silence the same gene reversibly.

This distinction has practical consequences. Mutations are generally irreversible and are inherited in a Mendelian fashion. Epigenetic changes can be reversed by enzymatic activity or pharmacological intervention, and they can be influenced by environmental factors. However, the line can blur: some mutations occur in genes encoding epigenetic machinery (such as DNMT3A or EZH2), and these mutations cause widespread epigenetic dysregulation. Conversely, epigenetic silencing of a DNA repair gene can lead to an increased mutation rate, creating a feedback loop between the two types of change. For a fuller treatment, see the [Difference Between Epigenetic and Genetic](/knowledge/molecular-biology/difference-between-epigenetic-and-genetic) discussion.

### Reversibility

Another misconception is that epigenetic marks are permanent. While some marks, such as those at constitutive heterochromatin, are remarkably stable, many epigenetic modifications are dynamically regulated. DNA methylation can be actively removed by ten-eleven translocation (TET) enzymes, which oxidize 5-methylcytosine to 5-hydroxymethylcytosine and further oxidation products, ultimately leading to replacement with unmethylated cytosine through [base excision repair](/knowledge/molecular-biology/base-excision-repair). Histone modifications are even more dynamic, with writers, erasers, and readers constantly acting on chromatin.

The reversibility of epigenetic marks is the basis for epigenetic therapies. HDAC inhibitors and DNMT inhibitors are approved for cancer treatment, and drugs targeting other epigenetic enzymes are in clinical development. However, reversibility should not be confused with instability—many epigenetic marks are faithfully maintained through hundreds of cell divisions, and reversing them often requires active intervention.

### Correlation vs. Causation

A third pitfall is assuming that an association between an epigenetic mark and a phenotype implies causation. Many studies report correlations between DNA methylation at specific loci and diseases such as cancer, obesity, or psychiatric disorders. However, these associations may reflect the consequence of the disease rather than its cause, or they may be confounded by cell-type composition differences between comparison groups.

For example, blood DNA methylation patterns differ between smokers and non-smokers at thousands of CpG sites, but most of these differences are likely consequences of smoking rather than causes of smoking-related diseases. Establishing causation requires functional experiments, such as targeted epigenetic editing using CRISPR-dCas9 fusion proteins, where a catalytically dead Cas9 is fused to a DNMT or a TET enzyme to introduce or remove methylation at a specific locus and observe the phenotypic consequences. Without such experiments, epigenetic associations should be interpreted cautiously.

## Summary and Key Takeaways

Epigenetic mechanisms provide the molecular basis for how identical genomes can produce diverse cell types and how environmental signals can leave lasting marks on gene expression. The four major mechanisms—DNA methylation, histone modification, chromatin remodeling, and non-coding RNA regulation—operate in an integrated network to establish and maintain gene expression programs.

- DNA methylation at CpG dinucleotides is the most stable epigenetic mark and is associated with gene silencing.
- Histone modifications, particularly acetylation and methylation, create a code of marks that recruit effector proteins and modulate chromatin structure.
- ATP-dependent chromatin remodelers slide, eject, or exchange nucleosomes to control access to DNA.
- Non-coding RNAs, including miRNAs and lncRNAs, regulate gene expression at multiple levels and can direct chromatin-modifying complexes to specific loci.
- Epigenetic marks are heritable through cell division but are also reversible, making them attractive therapeutic targets.
- The distinction between epigenetic changes and mutations is fundamental; epigenetic changes do not alter the DNA sequence.
- Epigenetic mechanisms are studied using bisulfite sequencing, ChIP-seq, and ATAC-seq, among other methods.
- X-inactivation, genomic imprinting, and cell differentiation are canonical examples of epigenetic regulation in action.

The study of [Epigenetic Modification](/knowledge/molecular-biology/epigenetic-modification) continues to reveal how [Epigenetic Factors](/knowledge/molecular-biology/epigenetic-factors) shape development, health, and disease, and how these effects can sometimes be transmitted across generations through [Epigenetic Inheritance](/knowledge/molecular-biology/epigenetic-inheritance). The [Epigenetic Theory](/knowledge/molecular-biology/epigenetic-theory) provides a framework for understanding how environmental exposures and stochastic events contribute to phenotypic variation beyond what the DNA sequence alone can explain.

## Frequently Asked Questions

### What are epigenetic mechanisms?

Epigenetic mechanisms are molecular processes that produce heritable changes in gene expression without altering the DNA sequence. The main types are DNA methylation, histone modification, chromatin remodeling, and regulation by non-coding RNAs. These mechanisms determine which genes are active or silent in a given cell and can be influenced by environmental factors.

### What is the meaning of epigenetic mechanisms?

The term "epigenetic" means "above" or "on top of" genetics. Epigenetic mechanisms are the molecular systems that control how the genetic code is read and interpreted. They package DNA into chromatin, mark specific genes for activation or silencing, and maintain these states through cell division.

### Can you give examples of epigenetic mechanisms?

Examples include DNA methylation of CpG islands in gene promoters, histone acetylation by HATs and deacetylation by HDACs, ATP-dependent nucleosome remodeling by SWI/SNF complexes, and gene silencing by XIST lncRNA during X-chromosome inactivation. Genomic imprinting, where genes are expressed from only one parental allele, is another example.

### How do epigenetic mechanisms work?

DNA methylation adds methyl groups to cytosine bases, recruiting proteins that compact chromatin and block transcription. Histone modifications alter the charge and binding properties of histone tails, affecting chromatin compaction and recruiting reader proteins. Chromatin remodelers use ATP to move or eject nucleosomes. Non-coding RNAs guide these modifying enzymes to specific genomic locations.

### What is the difference between genetics and epigenetics?

Genetics refers to the information encoded in the DNA sequence itself. Epigenetics refers to modifications that affect gene expression without changing the sequence. Genetic changes are permanent and inherited in a Mendelian fashion; epigenetic changes are often reversible and can be influenced by environmental factors.

### Are epigenetic changes reversible?

Yes. DNA methylation can be removed by TET enzymes, histone modifications are dynamically regulated by writers and erasers, and chromatin states can switch between active and silent configurations. This reversibility is exploited in cancer therapy with DNMT and HDAC inhibitors.

### What methods are used to study epigenetic mechanisms?

DNA methylation is studied using bisulfite sequencing, which distinguishes methylated from unmethylated cytosines. Histone modifications and protein-DNA interactions are mapped using chromatin immunoprecipitation followed by sequencing (ChIP-seq). Chromatin accessibility is measured using ATAC-seq, which uses the Tn5 transposase to identify open chromatin regions.

## Further Reading

- la Torre A, Lo Vecchio F, Greco A. *Epigenetic Mechanisms of Aging and Aging-Associated Diseases*. Cells. 2023. [PubMed 37190071](https://doi.org/10.3390/cells12081163)
- Sen P et al. *Epigenetic Mechanisms of Longevity and Aging*. Cell. 2016. [PubMed 27518561](https://doi.org/10.1016/j.cell.2016.07.050)
- Wu D et al. *Epigenetic mechanisms of Immune remodeling in sepsis: targeting histone modification*. Cell death & disease. 2023. [PubMed 36774341](https://doi.org/10.1038/s41419-023-05656-9)
- Li F et al. *Regulation of cisplatin resistance in bladder cancer by epigenetic mechanisms*. Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy. 2023. [PubMed 36774746](https://doi.org/10.1016/j.drup.2023.100938)
- Davie JR et al. *Basic Epigenetic Mechanisms*. Sub-cellular biochemistry. 2025. [PubMed 39820859](https://doi.org/10.1007/978-3-031-75980-2_1)
- Hayward S et al. *Epigenetic Mechanisms and Nephrotic Syndrome: A Systematic Review*. Biomedicines. 2023. [PubMed 36831050](https://doi.org/10.3390/biomedicines11020514)

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