Publication: Evolutionary trade-offs in kidney injury and repair
Authors
Lei, Yutian ; Anders, Hans Joachim
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-11-900
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info:eu-repo/semantics/article
Description
Abstract
Evolutionary medicine has proven helpful to
understand the origin of human disease, e.g. in
identifying causal roles of recent environmental changes
impacting on human physiology (environmentphenotype mismatch). In contrast, diseases affecting
only a limited number of members of a species often
originate from evolutionary trade-offs for usually
physiologic adaptations assuring reproductive success in
the context of extrinsic threats. For example, the G1 and
G2 variants of the APOL1 gene supporting control of
Trypanosoma infection come with the trade-off that they
promote the progression of kidney disease. In this
review we extend the concept of evolutionary
nephrology by discussing how the physiologic
adaptations (danger responses) to tissue injury create
evolutionary trade-offs that drive histopathological
changes underlying acute and chronic kidney diseases.
The evolution of multicellular organisms positively
selected a number of danger response programs for their
overwhelming benefits in assuring survival such as
clotting, inflammation, epithelial healing and
mesenchymal healing, i.e. fibrosis and sclerosis. Upon
kidney injury these danger programs often present as
pathomechanisms driving persistent nephron loss and
renal failure. We explore how classic kidney disease
entities involve insufficient or overshooting activation of
these danger response programs for which the
underlying genetic basis remains largely to be defined.
Dissecting the causative and hierarchical relationships
between danger programs should help to identify
molecular targets to control kidney injury and to
improve disease outcomes.
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