Posttranslational modifications in retinal degeneration diseases: An update on the molecular basis and treatment DOI Creative Commons
Ke Yao,

Qianxue Mou,

Zhen Jiang

и другие.

Brain‐X, Год журнала: 2024, Номер 2(3)

Опубликована: Сен. 1, 2024

Abstract Noninherited diseases and age‐associated vision loss are often associated with retinal degeneration. The retina is a postmitotic neural tissue lacking endogenous regeneration capacity. Therefore, understanding the mechanism of degeneration in pivotal. Posttranslational modifications (PTMs) determine protein function during physiological pathological processes, including signal transduction, localization, activation. Advanced detection technologies have revealed over 400 different PTMs acetylation, methylation, phosphorylation, ubiquitination SUMOylation. Here, we discuss to aid our their molecular basis suggest potential future clinical treatment.

Язык: Английский

The Role of Non-coding RNAs in Diabetic Retinopathy: Mechanistic Insights and Therapeutic Potential DOI

Zhuan Zuo,

Ni Li, Qian Zhang

и другие.

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0

Protein Acetylation in Age-Related Macular Degeneration: Mechanisms, Roles, and Therapeutic Perspectives DOI Creative Commons

Tian-Yi Luo,

Cunzi Li, Lan Zhou

и другие.

Investigative Ophthalmology & Visual Science, Год журнала: 2025, Номер 66(5), С. 30 - 30

Опубликована: Май 22, 2025

Age-related macular degeneration (AMD) is a top cause of severe vision loss and blindness in older adults globally. This multifactorial disease arises from genetic, environmental, age-related factors. Protein acetylation modification plays key role AMD progression through both epigenetic non-epigenetic pathways. review comprehensively discusses the multidimensional impacts protein AMD, particularly its dynamic regulation angiogenesis, oxidative stress, inflammatory responses, cellular senescence. Recent evidence shows that histone inhibits choroidal neovascularization (CNV) formation by regulating vascular endothelial growth factor (VEGF) hypoxia-inducible (HIF-1α) expression, while upregulating complement inhibitor clusterin to maintain Bruch's membrane integrity. Additionally, NAD+-dependent deacetylase SIRT1 modulates deacetylation transcription factors such as PGC-1α, NF-κB, FOXO3, enhancing mitochondrial antioxidant function suppressing cascades disrupt vicious cycle stress chronic inflammation. In terms senescence, hypoacetylation hyperacetylation non-histone proteins (e.g., p53, E2F1) jointly retinal pigment epithelial (RPE) cell-cycle arrest autophagy imbalance, accelerating progression. Genetic further reveals subtype-specific expression changes regulatory mechanisms deacetylases (HDACs), HDAC11 HDAC1/3, AMD. article explores clinical significance these findings proposes novel combined therapeutic strategy. It involves synergistically targeting homeostasis with HDAC inhibitors TSA, AN7) activators inhibiting abnormal repairing metabolic disorders, restoring function. dual-targeting approach may overcome current anti-VEGF therapy limitations open new precision management avenues for

Язык: Английский

Процитировано

0

Posttranslational modifications in retinal degeneration diseases: An update on the molecular basis and treatment DOI Creative Commons
Ke Yao,

Qianxue Mou,

Zhen Jiang

и другие.

Brain‐X, Год журнала: 2024, Номер 2(3)

Опубликована: Сен. 1, 2024

Abstract Noninherited diseases and age‐associated vision loss are often associated with retinal degeneration. The retina is a postmitotic neural tissue lacking endogenous regeneration capacity. Therefore, understanding the mechanism of degeneration in pivotal. Posttranslational modifications (PTMs) determine protein function during physiological pathological processes, including signal transduction, localization, activation. Advanced detection technologies have revealed over 400 different PTMs acetylation, methylation, phosphorylation, ubiquitination SUMOylation. Here, we discuss to aid our their molecular basis suggest potential future clinical treatment.

Язык: Английский

Процитировано

0