Emerging roles of autophagy in the stressed kidney allograft.
The transplanted kidney integrates a considerable number of tissular stress that challenge cell viability and promote inflammation and fibrogenesis. These injuries ultimately may lead to structural deterioration (ie, interstitial fibrosis and tubular atrophy) and to loss of function. In response to ischemic, toxic, or immunologic insults, which are the most frequent injuries encountered by transplanted kidneys, cells must adapt to maintain vital metabolic functions and to avoid death. Among the adaptive responses activated, autophagy has emerged as an important integrator of various extracellular and intracellular triggers (often related to nutrient availability or immunologic stimuli), which may in turn regulate cell viability and both innate and adaptive immune functions. This review provides an overview of the recent literature on the implications of autophagy in the field of kidney transplantation and discusses future directions for research.
INSERM U775 and Université Paris Descartes, Paris, France; and Service de Néphrologie, Hôpital Européen Georges Pompidou, Paris, France. Electronic address: npallet@yahoo.fr.
Nicolas
N
Pallet
D056704:Adaptive Immunity; D064591:Allografts; D000818:Animals; D001343:Autophagy / Q000502:physiology*; D006801:Humans; D007113:Immunity, Innate; D007166:Immunosuppressive Agents / Q000009:adverse effects; D007668:Kidney / Q000473:pathology*; D016030:Kidney Transplantation; D015427:Reperfusion Injury / Q000209:etiology; D013312:Stress, Physiological
D007166:Immunosuppressive Agents
Autophagy; cell stress; inflammation; kidney; transplantation