Research Progress on the Role of N6‑Methyladenosine in the

Development of Diabetes

Jingyi Huang

Chiway Repton High School, Xiamen, China

Keywords: N6‑methyladenosine (m6A), Diabetes Mellitus, RNA Methylation.

Abstract: N6-methyladenosine (m6A) is a key RNA modification widely found in eukaryotic mRNA, regulating RNA

stability, translation, splicing, and degradation. Recent studies highlight its critical role in diabetes

development by modulating insulin signaling, islet β-cell function, immune response, and lipid metabolism.

Additionally, m6A modification contributes to diabetic complications, such as retinopathy and nephropathy,

by influencing gene expression. Advances in technology have led to the identification of numerous diabetes-

related genes targeted by m6A, opening new therapeutic possibilities. Understanding the molecular

mechanisms of m6A in different diabetes types may aid in precision medicine approaches. This review

explores the potential of targeting m6A modification for early intervention and treatment, providing novel

insights into diabetes management. Future research on m6A's role in diabetes pathogenesis and complications

will enhance our ability to develop innovative therapeutic strategies, improving outcomes for diabetic

patients.

1 INTRODUCTION

Diabetes mellitus, especially type 2 diabetes mellitus

(T2DM), has become one of the major public health

problems in the world, and its incidence continues to

increase. According to the World Health

Organization (WHO), there are more than 400 million

people with diabetes worldwide, and this number is

still increasing (Zhang et al. 2022). Diabetes not only

affects the quality of life of patients, but also leads to

a variety of serious complications such as

cardiovascular disease, kidney disease, retinopathy,

which brings huge social and economic burden

(Tomic et al. 2022). Therefore, in-depth study of the

pathogenesis of diabetes and search for new

therapeutic targets and effective intervention

strategies are of great significance to reduce the

global burden of disease. In recent years, m6A (N6-

methyladenosine), as an important post-

transcriptional modification of RNA, has gradually

attracted wide attention. m6A modification is the

addition of a methyl group at the sixth position of the

nitrogen atom of adenosine molecule. This

modification plays an important role in gene

expression by regulating RNA stability, translation,

splicing and degradation. The regulation of m6A

modification is accomplished by a series of ‘write’

(e.g. METTL3, METTL14), ‘erase’ (e.g. FTO,

ALKBH5) and ‘read’ (e.g. YTHDF1, YTHDF2, etc.)

proteins (Wang et al. 2023). It is involved in cell

differentiation, proliferation, metabolic regulation

and immune response in physiological processes, and

plays a key role in a variety of pathological states,

especially in metabolic diseases such as cancer,

cardiovascular disease and diabetes. m6A

modification is closely related to the occurrence and

development of diabetes by regulating insulin

signaling, β-cell function, glucose metabolism and

inflammatory response (Liu et al. 2023).

Although several studies have explored the role

of N6-methyladenosine (m6A) modification in

diabetes, its precise mechanisms remain unclear. In

particular, how m6A influences different types of

diabetes, diabetic complications, and various cell

types is not yet fully understood. A comprehensive

review and analysis of existing literature on m6A

modification in diabetes is crucial for advancing our

knowledge of the disease at a molecular level.

Understanding its specific functions in insulin

signaling, β-cell function, immune regulation, and

metabolic pathways may help uncover new

therapeutic targets. Furthermore, m6A modification

appears to play a role in the progression of diabetic

180

Huang, J.

Research Progress on the Role of N6-Methyladenosine in the Development of Diabetes.

DOI: 10.5220/0014440300004933

Paper published under CC license (CC BY-NC-ND 4.0)

In Proceedings of the 1st International Conference on Biomedical Engineering and Food Science (BEFS 2025), pages 180-186

ISBN: 978-989-758-789-4

complications such as retinopathy and nephropathy

by regulating gene expression. Investigating these

mechanisms in greater detail could provide new

insights into disease pathology and potential

treatment strategies. As research in this field

progresses, targeting m6A modification may pave

the way for precision medicine approaches,

enabling more effective and personalized diabetes

treatments. By systematically summarizing current

findings and identifying gaps in knowledge, future

studies can focus on unraveling the complexities of

m6A in diabetes, ultimately leading to innovative

therapeutic advancements. Continued exploration

of this modification holds promise for improving

early intervention and treatment outcomes in

diabetic patients.

2 THE ROLE OF M6A

MODIFICATIONS IN THE

PATHOGENESIS OF

DIABETES MELLITUS

2.1 The Regulation of the Insulin

Signaling Pathway by m6A

Modification

The N6-methyladenosine (m6A) modification of

mRNA has been proposed to play a vital role in the

progression of type 2 diabetes (T2D) (De Jesus et al.

2019). In Li's research, it was discovered that m6A

modification is related to the regulation of the insulin

signaling pathway (Li et al. 2023). KEGG enrichment

analysis revealed that the downregulated MP-DEGs

were primarily enriched in the insulin signaling, IR,

and AMPK signaling pathways. Additional studies

have shown that AMPK plays a major role in

regulating cellular energy balance. Therefore, the

results found by Li's team indicate that the

development of IR and T2D may be regulated by

these metabolism-related proteins through their

interference with the insulin signaling pathway or

energy balance.

2.2 The Role of m6A Modification in

Pancreatic β-Cell Function

The role of m6A modification in islet β-cell function

has been investigated (Regué et al. 2021). In that

study, researchers discovered that deletion of IMP2 in

pancreatic β-cells leads to reduced compensatory β-

cell proliferation and function. Mechanistically,

IMP2 directly binds to Pdx1 mRNA and stimulates its

translation in an m6A-dependent manner.

Furthermore, IMP2 orchestrates the IGF2-AKT-

GSK3β-PDX1 signaling pathway to stabilize PDX1

polypeptides. In human EndoC-βH1 cells,

overexpression of IMP2 enhances cell proliferation,

PDX1 protein levels, and insulin secretion. Another

study illustrated that m6A methylation is essential for

β-cell maturation and maintenance of their

physiological function (Zhou et al. 2022). The

relationship between METTL3-mediated m6A RNA

methylation and H2O2-induced pancreatic β-cell

apoptosis was also demonstrated. It was shown that

H2O2 induces β-cell apoptosis by reducing METTL3

expression, while exenatide, which targets METTL3,

restores m6A levels, thereby reversing H2O2-

induced β-cell injury.

2.3 The Relationship between m6A

Modification and Metabolic

Regulation

The relationship between m6A modification and

metabolic regulation has been analyzed (Zhang et al.

2021). In patients with type 2 diabetes (T2D), glucose

levels play a crucial role in the dynamic regulation of

N6-methyladenosine (m6A) modification.

Specifically, elevated glucose levels can

simultaneously reduce the mRNA expression of FTO,

an important m6A demethylase, while increasing the

expression of key methyltransferases, including

METTL3, METTL14, and WTAP. These enzymes

are responsible for catalyzing m6A methylation,

which affects RNA stability, translation, and overall

gene expression. The simultaneous decrease in FTO

and increase in methyltransferases contribute to

altered m6A patterns, ultimately impacting insulin

signaling and metabolic processes. These molecular

changes are critical in maintaining glucose

homeostasis in T2D patients, influencing β-cell

function and systemic glucose metabolism.

Understanding the regulatory effects of glucose on

m6A modification may provide new insights into

diabetes progression and potential therapeutic

strategies. Further research into this dynamic

interplay could lead to the development of targeted

treatments for better glycemic control in T2D

patients.

Research Progress on the Role of N6-Methyladenosine in the Development of Diabetes

181

3 THE RELATIONSHIP

BETWEEN M6A

MODIFICATION AND

DIABETIC COMPLICATIONS

3.1 The Relationship between m6A

Modification and Diabetic

Retinopathy

The relationship between m6Amodification and

diabetic retinopathy has been analyzed (Kumari et al.

2021). Researchers discovered that m6ARNA

modification exerts its effects through its writer,

reader, and eraser proteins. Although limited research

has been conducted on the role of m6ARNA

modification in diabetic retinopathy (DR), its

involvement in inflammation, oxidative stress,

angiogenesis, various coding and non-coding RNAs,

neurogenesis, diabetes, and its risk factors, as well as

other molecular pathways, suggests that it is a

potential candidate for targeting the study and control

of DR progression and pathogenesis. Another study

also delved deeply into the relationship between

m6Amodification and diabetic complications (Benak

et al. 2023). In retinal pigment epithelium (RPE)

cells, high-glucose conditions downregulated the

expression of METTL3 at both the transcript and

protein levels. Further experiments showed that

METTL3 overexpression alleviated the cytotoxic

effects of high glucose on RPE cells, while METTL3

depletion had the opposite effect. Conversely,

diabetic stress induced upregulation of METTL3 and

a subsequent increase in m6Alevels in human retinal

pericytes and mouse retinas. Specific depletion of

METTL3 in pericytes suppressed diabetes-induced

pericyte dysfunction and vascular complications in

vivo. A recent study demonstrated downregulation of

METTL3 in vitreous humor samples from patients

with DR, in a mouse model of DR, and in high

glucose-induced human retinal microvascular

endothelial cells.

3.2 The Relationship between m6A

Modification and Diabetic

Nephropathy

The relationship between m6Amodification and

diabetic nephropathy (DN) was investigated by a

research team (Wan et al. 2022). They analyzed the

m6Acontent in the urine of patients with DN and

found that m6Alevels were significantly lower in

patients with DN compared to those with normal

glucose tolerance (NGT) and patients with type 2

diabetes mellitus (T2DM). The team further explored

the changes in m6Alevels across different stages of

DN progression and discovered that m6Alevels

continued to decrease as DN worsened, closely

correlating with the presence of DN. They also found

that m6Alevels decreased gradually with the

progression of DN, highlighting its close association

with the pathological process of DN. Urinary

m6Alevels were negatively correlated with

pancreatic islet and renal function indices, suggesting

that m6Ais a potential independent risk factor for DN

and is linked to diabetic kidney dysfunction.

3.3 The Relationship between m6A

Modification and Diabetic

Cardiovascular Complications

The relationship between m6Amodification and

cardiovascular complications in diabetes has been

analyzed (Qin et al. 2020). m6Amethylation is

present across different species and plays a

fundamental role in cardiac biological processes and

the pathogenesis of cardiovascular diseases (CVD).

An increasing number of studies have uncovered the

dysregulation of m6Amethylation as a hallmark of

CVD development. m6Amodification can either

promote or inhibit the development of CVD by

regulating the levels of targeted m6A-modified

mRNAs. Dysregulation of methyltransferases,

demethylases, and m6A-binding proteins has been

shown to contribute to the onset and progression of

CVD.

4 M6A MODIFICATION AS A

NEW THERAPEUTIC TARGET

FOR DIABETES

4.1 Therapeutic Strategies Targeting

m6A ‘Writer’ Enzymes

Therapeutic strategies targeting m6A ‘writer’

enzymes, such as METTL3 and METTL14, have

been analyzed (Qiu et al. 2023). The

methyltransferase complex is composed of METTL3

and METTL14. METTL3, which contains an active

methyltransferase domain, transfers a methyl group

from S-adenosylmethionine to the adenosine residue

on the substrate. METTL14, a critical component,

supports METTL3 in recognizing RNA substrates.

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The m6Amodification site is particularly localized at

the beginning of the 3’untranslated region, near the

stop codon, and is typically embedded within the

consensus motif 5’-RRACH-3’. The METTL3-

METTL14 heterodimer binds to WTAP, which acts

as an adaptor protein interacting with the

methyltransferases, even though it lacks catalytic

methylation activity.

4.2 Therapeutic Strategies Targeting

m6A ‘Eraser’ Enzymes

Therapeutic strategies targeting m6A ‘eraser’

enzymes, such as FTO and ALKBH5, have been

discussed (Zhang et al. 2021). FTO plays a key role

in RNA methylation modifications, including cap

m6Am and m1A, with varying efficiency. Its

subcellular localization influences substrate

specificity. In the nucleus, FTO preferentially

demethylates internal m6A in poly(A) RNA, m6A

and m6Am in small nuclear RNA (snRNA), and m1A

in transfer RNA (tRNA). In the cytoplasm, it

demethylates both internal m6A and cap m6Am in

poly(A) RNA, as well as m1A in tRNA. The crystal

structure of FTO bound to 6mA-modified single-

stranded DNA (ssDNA) reveals the molecular basis

for its recognition and catalytic demethylation of

different substrates. This structural insight

demonstrates that N6-methyladenine is the most

favorable nucleobase substrate for FTO.

Understanding FTO’s role in RNA modifications and

its substrate specificity provides valuable insights

into its function in gene regulation and cellular

processes, which may have implications for various

diseases, including diabetes.

4.3 m6A Modification and the

Application of Small Molecule

Drugs

The application of m6Amodification in combination

with diabetes drugs has been investigated (Zhou et al.

2024). Zhou’s team explored the potential role of

metformin in m6Amodification in NIT-1 cells by

quantifying the m6Acontent in these cells. They

found that treatment with H2O2 led to a significant

reduction in m6Amethylation levels compared to

cells treated with metformin. Additionally, the

mRNA expressions of the m6Amethyltransferases

METTL3 and METTL14 were decreased in NIT-1

cells treated with H2O2, while no noticeable changes

were observed in the mRNA levels of the

m6Ademethylases FTO and ALKBH5. Interestingly,

metformin treatment increased the degree of

m6Amethylation in the H2O2-treated group and

partially restored the mRNA expression of

METTL14, although it did not significantly impact

the mRNA levels of METTL3 or FTO. Furthermore,

Western blot analysis demonstrated that metformin

treatment enhanced the protein level of METTL14.

5 RESEARCH PROGRESS AND

CHALLENGES

5.1 Complexity and Context-

Dependent Effects of m6A

One of the most significant challenges in studying

m6A modifications is their complex and context-

dependent effects. The consequences of m6A

modification can vary depending on the specific RNA

molecule, cell type, and physiological condition. For

example, in pancreatic β-cells, m6A has been shown

to regulate insulin mRNA stability and translation

efficiency, but its effects can differ under conditions

of hyperglycemia or insulin resistance.

Understanding the precise role of m6A in different

metabolic tissues and disease states is essential but

remains a significant challenge due to the dynamic

nature of this modification (Shi et al. 2019).

5.2 Lack of Specific and Potent Small

Molecule Modulators

While some small molecule inhibitors and activators

of m6A regulators have been identified, their

specificity and potency remain major limitations.

Many currently available inhibitors, such as Rhein

(an FTO inhibitor) and STM2457 (a METTL3

inhibitor), exhibit off-target effects that may lead to

unwanted metabolic disturbances. Additionally, the

development of highly selective small molecules

targeting specific m6A-modifying enzymes without

affecting other RNA modifications is still in its early

stages (Gu et al. 2020).

5.3 Limited Understanding of m6A

Regulatory Networks in Diabetes

The interplay between m6A modifications and key

metabolic pathways in diabetes remains poorly

understood. Although m6A modifications regulate

mRNA stability, splicing, and translation, how these

processes interact with insulin signaling pathways,

Research Progress on the Role of N6-Methyladenosine in the Development of Diabetes

183

glucose metabolism, and inflammatory responses is

still being explored. Moreover, the roles of m6A

readers (e.g., YTHDF1, YTHDF2) in mediating

downstream effects are not fully elucidated, making

it challenging to design targeted therapeutic

interventions (Du et al. 2022).

5.4 Technical Limitations in m6A

Detection and Quantification

Despite advancements in m6A sequencing

technologies (e.g., MeRIP-seq, m6A-CLIP),

challenges remain in accurately mapping m6A

modifications at single-nucleotide resolution. Many

current methods have limited sensitivity and

specificity, making it difficult to distinguish

functionally relevant m6A sites from background

noise. Furthermore, the requirement for large

amounts of RNA and the complexity of

bioinformatics analysis hinder widespread adoption

in clinical and translational research (Motorin et al.

2023).

5.5 Safety and Long-Term Effects of

m6A-Targeting Therapies

The long-term effects of modulating m6A

modifications are still not fully understood. Given

that m6A plays a vital role in various physiological

processes such as cell differentiation, immune

responses, and neuronal function, any therapeutic

intervention targeting m6A pathways requires careful

evaluation for potential side effects. m6A

modifications regulate gene expression, RNA

stability, and protein synthesis, all of which are

essential for normal cellular functions. Therefore,

disrupting m6A homeostasis could have unintended

consequences. For instance, it may impair immune

function, leading to increased susceptibility to

infections or autoimmune diseases. Additionally,

alterations in m6A regulation could elevate cancer

risk by influencing the expression of oncogenes or

tumor suppressor genes. Furthermore, m6A

dysfunction during development may result in

abnormalities in cell differentiation and tissue

formation, potentially causing developmental defects.

As research progresses, it is crucial to understand the

full scope of m6A's impact on health and disease.

Long-term safety studies will be necessary before

m6A-targeted therapies can be widely used, ensuring

their benefits outweigh potential risks (Faraj et al.

2023).

6 FUTURE RESEARCH

DIERECTION

6.1 Development of Highly Selective

Small Molecule Modulators

Future research should prioritize the design of highly

selective and potent small molecule inhibitors or

activators of m6A-related enzymes. By leveraging

structure-based drug design and high-throughput

screening techniques, researchers can identify novel

compounds with enhanced specificity, minimizing

off-target effects. These approaches could enable the

development of therapeutic agents that precisely

modulate m6A pathways, offering new treatment

options for diseases associated with m6A

dysregulation, such as cancer, diabetes, and

neurological disorders. Additionally, the

development of targeted drug delivery systems,

including nanoparticle-based strategies, could

improve the therapeutic efficacy of m6A modulators

by ensuring more localized action and reducing

systemic toxicity. Such systems would allow for the

precise delivery of these compounds to specific

tissues or cell types, maximizing their beneficial

effects while minimizing potential side effects.

Ultimately, these advancements could lead to safer,

more effective therapies for conditions driven by

abnormal m6A regulation, offering promising new

avenues for precision medicine (Deng et al. 2022).

6.2 Comprehensive Mapping of m6A

Regulatory Networks

To fully understand the role of m6A in diabetes,

researchers must map its entire regulatory network

across key metabolic tissues, including the pancreas,

liver, adipose tissue, and skeletal muscle. These

tissues play essential roles in glucose metabolism and

insulin signaling, making them critical for studying

diabetes progression. Advanced techniques, such as

single-cell RNA sequencing combined with m6A

profiling, offer powerful tools to investigate cell-

type-specific m6A modifications. These approaches

can provide deeper insights into how m6A

dynamically regulates gene expression in different

tissues, influencing insulin production, glucose

uptake, and lipid metabolism. By identifying the

specific roles of m6A in various cell types,

researchers can uncover new mechanisms underlying

diabetes development and its complications.

Understanding these regulatory pathways may lead to

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novel therapeutic strategies targeting m6A

modifications to improve diabetes management.

Future studies focusing on tissue-specific m6A

patterns could pave the way for precision medicine

approaches in diabetes treatment (Zhang et al. 2019).

7 CONCLUSION

N6-methyladenosine (m6A) is a key post-

transcriptional RNA modification widely found in

eukaryotic mRNA, influencing RNA stability,

translation, splicing, and degradation. Recent

research highlights its significant role in diabetes,

particularly type 2 diabetes (T2D), by regulating

insulin signaling, islet β-cell function, immune

response, and lipid metabolism. However, despite

growing evidence, the precise mechanisms of m6A in

diabetes and its complications remain unclear,

especially its effects across different diabetes types,

cell types, and complications such as diabetic

retinopathy and nephropathy. Glucose levels

dynamically regulate m6A modification in T2D

patients. High glucose concentrations lead to reduced

expression of FTO, a key m6A demethylase, while

simultaneously increasing the expression of

METTL3, METTL14, and WTAP, the primary

methyltransferases involved in m6A modification.

These molecular changes significantly affect insulin

signaling and metabolic pathways, contributing to

glucose homeostasis and diabetes progression.

Advances in technology have identified numerous

diabetes-related genes targeted by m6A, offering

promising therapeutic opportunities. Given the

complexity of m6A’s involvement in diabetes,

systematically reviewing and summarizing existing

studies can deepen our understanding of its molecular

mechanisms. A better grasp of how m6A

modifications regulate key genes could pave the way

for precision treatments aimed at improving diabetes

management. As research progresses, targeting m6A-

related pathways may provide novel intervention

strategies, enhancing therapeutic outcomes for

diabetic patients. Exploring this modification in

greater depth could lead to more effective,

personalized treatment approaches. Future studies

should focus on elucidating the specific roles of m6A

in different diabetes subtypes and complications. By

bridging current knowledge gaps, researchers can

develop innovative therapies based on m6A

modifications, potentially revolutionizing early

intervention and treatment strategies for diabetes and

its related complications.

REFERENCES

Benak, D., Benakova, S., & Plecita-Hlavata, L., et al. 2023.

The role of m6A and m6Am RNA modifications in the

pathogenesis of diabetes mellitus. Frontiers in

Endocrinology 14:6-7.

De Jesus, D. F., Zhang, Z., & Kahraman, S., et al. 2019.

m6A mRNA methylation regulates human β-cell

biology in physiological states and in type 2 diabetes.

Nature Metabolism 1(8):765–769.

Deng, L. J., Deng, W. Q., & Fan, S. R., et al. 2022. m6A

modification: recent advances, anticancer targeted drug

discovery and beyond. Molecular Cancer 21(1):13-15.

Du, R., Bai, Y., & Li, L. 2022. Biological networks in

gestational diabetes mellitus: insights into the

mechanism of crosstalk between long non-coding RNA

and N6-methyladenine modification. BMC Pregnancy

and Childbirth 22(1):7-11.

Faraj, R., Liang, Y., & Feng, A., et al. 2023. Exploring

m6A‐RNA methylation as a potential therapeutic

strategy for acute lung injury and acute respiratory

distress syndrome. Pulmonary Circulation 13(2):11-13.

Gu, J., Xu, J., &You, Q., et al. 2020. Recent developments

of small molecules targeting RNA m6A modulators.

European Journal of Medicinal Chemistry 196:5-7.

Kumari, N., Karmakar, A., & Khan, M. M. A., et al. 2021.

The potential role of m6A RNA methylation in diabetic

retinopathy. Experimental Eye Research 208:55-59.

Li, Y. L., Li, L., & Liu, Y. H.,et al. 2023. Identification of

metabolism-related proteins as biomarkers of insulin

resistance and potential mechanisms of m6A

modification. Nutrients 15(8):15-17.

Liu, Y., Yang, D., & Liu, T., et al. 2023. N6-

methyladenosine-mediated gene regulation and

therapeutic implications. Trends in Molecular Medicine

29(6):454-459.

Motorin, Y. & Helm, M. 2023. General principles and

limitations for detection of RNA modifications by

sequencing. Accounts of Chemical Research

57(3):280-285.

Qin, Y., Li, L., & Luo, E., et al. 2020. Role of m6A RNA

methylation in cardiovascular disease. International

Journal of Molecular Medicine 46(6):1962-1965.

Qiu, L., Jing, Q., & Li, Y., et al. 2023. RNA modification:

mechanisms and therapeutic targets. Molecular

Biomedicine 4(1):2-4.

Regué, L., Zhao, L., & Ji, F., et al. 2021. RNA m6A reader

IMP2/IGF2BP2 promotes pancreatic β-cell

proliferation and insulin secretion by enhancing PDX1

expression. Molecular Metabolism 48:4-7.

Shi, H., Wei, J., & He, C. 2019. Where, when, and how:

context-dependent functions of RNA methylation

writers, readers, and erasers. Molecular Cell 74(4):643-

647.

Tomic, D., Shaw, J. E., & Magliano, D. J. 2022. The burden

and risks of emerging complications of diabetes

mellitus. Nature Reviews Endocrinology 18(9):525-

529.

Research Progress on the Role of N6-Methyladenosine in the Development of Diabetes

185

Wan, S. J., Hua, Q., & Xing, Y. J., et al. 2022. Decreased

urine N6-methyladenosine level is closely associated

with the presence of diabetic nephropathy in type 2

diabetes mellitus. Frontiers in Endocrinology 13:6-9.

Wang, W., Wang, H., & Sun, T. 2023. N6-methyladenosine

modification: Regulatory mechanisms and therapeutic

potential in sepsis. Biomedicine & Pharmacotherapy

168:3-6.

Zhang, S. Y., Zhang, S. W., & Fan, X. N., et al. 2019.

Global analysis of N6-methyladenosine functions and

its disease association using deep learning and network-

based methods. PLoS Computational Biology 15(1):11-

16.

Zhang, W., Qian, Y., & Jia, G. 2021. The detection and

functions of RNA modification m6A based on m6A

writers and erasers. Journal of Biological Chemistry

297(2):2-7.

Zhang, W., Zhang, S., & Dong, C., et al. 2022. A

bibliometric analysis of RNA methylation in diabetes

mellitus and its complications from 2002 to 2022.

Frontiers in Endocrinology 13:2-4.

Zhang, Y., Chen, W., & Zheng, X., et al. 2021. Regulatory

role and mechanism of m6A RNA modification in

human metabolic diseases. Molecular Therapy-

Oncolytics 22:52-63.

Zhou, S., Sun, Y., & Xing, Y., et al. 2022. Exenatide

ameliorates hydrogen peroxide-induced pancreatic β-

cell apoptosis through regulation of METTL3-mediated

m6A methylation. European Journal of Pharmacology

924:3-8.

Zhou, S. M., Yao, X. M., & Cheng, Y., et al. 2024.

Metformin enhances METTL14-mediated m6A

methylation to alleviate NIT-1 cells apoptosis induced

by hydrogen peroxide. Heliyon 10(2):5-9.

BEFS 2025 - International Conference on Biomedical Engineering and Food Science

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