| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 4088 |
Name | SMAD3 |
Synonymous | SMAD family member 3;SMAD3;SMAD family member 3 |
Definition | MAD homolog 3|MAD, mothers against decapentaplegic homolog 3|SMA- and MAD-related protein 3|SMAD, mothers against DPP homolog 3|hMAD-3|hSMAD3|mad homolog JV15-2|mad protein homolog|mad3|mothers against DPP homolog 3|mothers against decapentaplegic homolog |
Position | 15q22.33 |
Gene type | protein-coding |
Title | Abstract |
| Cellular senescence: from physiology to pathology. | Recent discoveries are redefining our view of cellular senescence as a trigger of tissue remodelling that acts during normal embryonic development and upon tissue damage. To achieve this, senescent cells arrest their own proliferation, recruit phagocytic immune cells and promote tissue renewal. This sequence of events - senescence, followed by clearance and then regeneration - may not be efficiently completed in aged tissues or in pathological contexts, thereby resulting in the accumulation of senescent cells. Increasing evidence indicates that both pro-senescent therapies and antisenescent therapies can be beneficial. In cancer and during active tissue repair, pro-senescent therapies contribute to minimize the damage by limiting proliferation and fibrosis, respectively. Conversely, antisenescent therapies may help to eliminate accumulated senescent cells and to recover tissue function. |