6533b85efe1ef96bd12bfc65

RESEARCH PRODUCT

BCL-xL, a Mitochondrial Protein Involved in Successful Aging: From C. elegans to Human Centenarians

Marta InglesJose ViñaAurora Román-domínguezJuan GambiniConsuelo BorrasJorge Sanz-rosCristina Mas BarguesLucia Gimeno-mallench

subject

SenescenceautophagyAgingProgrammed cell deathsenescencemedia_common.quotation_subjectbcl-X ProteinBcl-xLReviewMitochondrionInhibitor of apoptosisCatalysislcsh:ChemistryMitochondrial ProteinsInorganic Chemistry03 medical and health sciences0302 clinical medicinelongevityAnimalsHumansPhysical and Theoretical ChemistryCaenorhabditis eleganslcsh:QH301-705.5Molecular BiologySpectroscopy030304 developmental biologymedia_commonAged 80 and over0303 health sciencesbiologyOrganic ChemistryAutophagyapoptosisLongevityGeneral MedicineComputer Science ApplicationsCell biologymitochondriaCrosstalk (biology)lcsh:Biology (General)lcsh:QD1-999healthy aging030220 oncology & carcinogenesisbiology.proteinFisiologia humana

description

B-Cell Lymphoma-extra-large (BCL-xL) is involved in longevity and successful aging, which indicates a role for BCL-xL in cell survival pathway regulation. Beyond its well described role as an inhibitor of apoptosis by preventing cytochrome c release, BCL-xL has also been related, indirectly, to autophagy and senescence pathways. Although in these latter cases, BCL-xL has dual roles, either activating or inhibiting, depending on the cell type and the specific conditions. Taken together, all these findings suggest a precise mechanism of action for BCL-xL, able to regulate the crosstalk between apoptosis, autophagy, and senescence, thus promoting cell survival or cell death. All three pathways can be both beneficial or detrimental depending on the circumstances. Thus, targeting BCL-xL would in turn be a 'double-edge sword' and therefore, additional studies are needed to better comprehend this dual and apparently contradictory role of BCL-XL in longevity. View Full-Text Keywords: healthy aging; apoptosis; autophagy; senescence; longevity; mitochondria

https://doi.org/10.3390/ijms21020418