Post-translational modifications of histone and non-histone proteins in epigenetic regulation and translational applications in alcohol-associated liver disease: Challenges and research opportunities

Rungratanawanich, Wiramon; Ballway, Jacob W.; Wang, Xin; Won, Kyoung-Jae; Hardwick, James P.; Song, Byoung-Joon

doi:10.1016/j.pharmthera.2023.108547

Cited by 5 publications

(2 citation statements)

References 349 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Histone methylation refers to the transfer of up to three methyl groups from the common methyl donor S‐adenosyl‐L‐methionine (SAM) to lysine or arginine residues of histones (Horiuchi et al., 2013 ; Rungratanawanich et al., 2023 ). Histone methyltransferases can be generally classified into three different classes: SET domain‐containing N‐lysine methyltransferases, disruptor of telomeric silencing 1‐like (DOT1L) with lysine as its substrate, and protein arginine transferases (PRMTs) which result in methylation of arginine (Horiuchi et al., 2013 ; Zhou et al., 2022 ).…”

Section: How Do Hallmarks Of Aging Participate In the Pathogenesis Of...mentioning

confidence: 99%

Osteoclasts and osteoarthritis: Novel intervention targets and therapeutic potentials during aging

Wang,

Yuan,

Wang

et al. 2024

Aging Cell

View full text Add to dashboard Cite

Osteoarthritis (OA), a chronic degenerative joint disease, is highly prevalent among the aging population, and often leads to joint pain, disability, and a diminished quality of life. Although considerable research has been conducted, the precise molecular mechanisms propelling OA pathogenesis continue to be elusive, thereby impeding the development of effective therapeutics. Notably, recent studies have revealed subchondral bone lesions precede cartilage degeneration in the early stage of OA. This development is marked by escalated osteoclast‐mediated bone resorption, subsequent imbalances in bone metabolism, accelerated bone turnover, and a decrease in bone volume, thereby contributing significantly to the pathological changes. While the role of aging hallmarks in OA has been extensively elucidated from the perspective of chondrocytes, their connection with osteoclasts is not yet fully understood. There is compelling evidence to suggest that age‐related abnormalities such as epigenetic alterations, proteostasis network disruption, cellular senescence, and mitochondrial dysfunction, can stimulate osteoclast activity. This review intends to systematically discuss how aging hallmarks contribute to OA pathogenesis, placing particular emphasis on the age‐induced shifts in osteoclast activity. It also aims to stimulate future studies probing into the pathological mechanisms and therapeutic approaches targeting osteoclasts in OA during aging.

show abstract

Section: How Do Hallmarks Of Aging Participate In the Pathogenesis Of...mentioning

confidence: 99%

Osteoclasts and osteoarthritis: Novel intervention targets and therapeutic potentials during aging

Wang,

Yuan,

Wang

et al. 2024

Aging Cell

View full text Add to dashboard Cite

show abstract

“…These epigenetic effects are caused by the activities of DNA methylases and chromatin modification enzymes, as reviewed by Jaenisch and Bird 2003 [ 2 ]. Changes in epigenetic factors may arise from the altered expressions of DNA methylation or histone modification enzymes, which can often lead to diseases, including cancer [ 3 ].…”

mentioning

confidence: 99%