Publications by authors named "Changjiao Luan"
Background: Accumulation of senescent cells in tissues and their downstream effect programs have emerged as key drivers of aging and age-associated pathologies. Recent progresses in senotherapeutics indicated that either selectively killing senescent cells with senolytics or suppressing the senescence-associated secretory phenotype (SASP) secretion using senomorphics contributes to extending of the healthy lifespan and alleviating numerous age-related disorders in mice.
Purpose: However, the potential side-effects and long-term cytotoxicity of the above novel compounds have not yet been determined.
Backgrounds: With the increasing demand for beauty and a healthy lifespan, studies regarding anti-skin aging have drawn much more attention than ever before. Skin cellular senescence, the primary cause of skin aging, is characterized by a cell cycle arrest in proliferating cells along with a senescence-associated secretory phenotype (SASP), which can be triggered by various internal or external stimuli.
Aims: Recent studies have made significant progress in the fields of anti-senescence and anti-aging.
Article Synopsis
- Senescent cells are non-dividing cells associated with skin aging due to a specific secretory phenotype, but understanding skin aging has been limited by a lack of identified markers.
- Recent research indicates that intracellular calcium signaling is important in regulating cellular senescence, especially in skin keratinocytes, although its exact roles are still not fully understood.
- This study developed a model of skin keratinocyte senescence using ionizing radiation and found that inhibiting the calcium-related gene TGM2 can delay senescence by reducing calcium signaling, oxidative stress, DNA damage, and inflammatory secretions.
Senescent cells are known to be accumulated in aged organisms. Although the two main characteristics, cell cycle arrest (for dividing cells) and secretion of senescence-associated secretory phenotype (SASP) factors, have been well described, the lack of sufficient senescent markers and incomplete understanding of mechanisms have limited the progress of the anti-senescence field. Calcium transferred from the endoplasmic reticulum (ER) via inositol 1, 4, 5-trisphosphate receptor type 2 (ITPR2) to mitochondria has emerged as a key player during cellular senescence and aging.
View Article and Find Full Text PDFCellular senescence is broadly known as a stable cell cycle arrest accompanied by a senescence-associated secretory phenotype (SASP). In the past decades, calcium signaling has emerged as a key mediator of cellular senescence. However, the transcriptional regulation of calcium signaling during cellular senescence remains partially understood.
View Article and Find Full Text PDFBackground: Traumatic brain injury (TBI) has emerged as an increasing public health problem but has not been well studied, particularly the mechanisms of brain cellular behaviors during TBI.
Methods: In this study, we established an ischemia/reperfusion (I/R) brain injury mice model using transient middle cerebral artery occlusion (tMCAO) strategy. After then, RNA-sequencing of frontal lobes was performed to screen key inducers during TBI.