Caspase5driven

Caspase5driven describes cellular responses predominantly mediated by caspase-5, a human inflammatory caspase homologous to murine caspase-11. In humans, caspase-5 participates in noncanonical inflammasome signaling, typically activated by cytosolic lipopolysaccharide (LPS) detection. Upon activation, caspase-5 cleaves gasdermin D, producing an N-terminal fragment that forms pores in the plasma membrane, triggering pyroptosis and the release of intracellular contents and inflammatory mediators.

In addition to pore formation, caspase-5 activity can promote downstream inflammatory signaling, including the maturation and release of cytokines such as IL-1β and IL-18, either directly or by facilitating activation of the canonical inflammasome. Caspase-5 can act in parallel with caspase-1 or influence its activation, depending on the cellular context. The term “caspase5driven” is used to emphasize the central role of caspase-5 in initiating these events, though research often refers to the broader noncanonical inflammasome pathway involving caspase-4/5.

Regulation of caspase-5 occurs at transcriptional and post-translational levels and is influenced by innate immune signals, including interferons and TLR pathways. Dysregulation of caspase-5–driven responses has been linked to inflammatory and autoinflammatory conditions, sepsis, and various infectious diseases in experimental models and clinical studies.

Given ongoing research, the exact delineation of caspase-5–driven pathways can vary by tissue type and stimulus. Caspase-5 remains a focus of investigation for understanding noncanonical inflammasome biology and potential therapeutic targeting.