Our team is best known for the discovery that, in programmed cell death (apoptosis), mitochondrial membrane permeabilization constitutes the point-of-no-return of the lethal process and thus defines the apoptotic checkpoint. Later, we provided an operational definition of "mitotic catastrophe" as an oncosuppressive mechanism, launched the debate that necrosis may be a regulated cell death event, and showed that autophagy usually is a cytoprotective event that avoids cell death and actually prolongs longevity when it is induced at the whole-organism level. We deciphered part of the molecular crosstalk between apoptosis and autophagy. We identified spermidine as a novel, non-toxic inducer of autophagy and determined its mode of action as a life span-extending drug. We launched the (still valid) hypothesis that all longevity extending manipulations, be they pharmacological or genetic, must induce autophagy to be efficient. Recently, we invalidated the dogma that apoptosis is a non-immunogenic cell death modality. We demonstrated that, depending on the upstream triggers, apoptosis can be immunogenic and hence alert the innate immune system and instruct it to stimulate a cognate response against dead-cell antigens. This has opened a new field of research at the frontier between immunology and cell biology, allowing us to define the molecular properties of immunogenic cell death. Our current research projects are designed to discover the pathophysiological implications of cell death, mostly in the context of cancer and immunosurveillance.
Website: http://www.kroemerlab.com/Members involved in CoLoMoTo activities:
- Gautier Stoll