Ischemia causes AKI as a result of ATP depletion, and rapid recovery of ATP on reperfusion
is important to minimize tissue damage. ATP recovery is often delayed, however, because …

The burst of reactive oxygen species (ROS) during reperfusion of ischemic tissues can
trigger the opening of the mitochondrial permeability transition (MPT) pore, resulting in …

Microvascular rarefaction, or loss of microvascular density, is increasingly implicated in the
progression from acute ischemic kidney injury to chronic kidney disease. Microvascular …

A decline in energy is common in aging, and the restoration of mitochondrial bioenergetics
may offer a common approach for the treatment of numerous age‐associated diseases …

The innate immune system has been implicated in both AKI and CKD. Damaged
mitochondria release danger molecules, such as reactive oxygen species, DNA, and …

Kidney ischemia–reperfusion (I/R) injury elicits cellular injury in the proximal tubule, and
mitochondrial dysfunction is a pathological consequence of I/R. Promoting mitochondrial …

Mitochondrial biogenesis occurs under basal conditions and is an adaptive response
initiated by cells to maintain energetic demands and metabolic homeostasis after injuries …

Acute kidney injury (AKI) is a common clinical disorder associated with decline in renal
function because of ischemic and nephrotoxic insults. The pathophysiology of AKI involves …

Mitochondrial dysfunction contributes to cardiac pathologies. Barriers to new therapies
include an incomplete understanding of underlying molecular culprits and a lack of effective …

Mitochondrial dysfunction underlies the etiology of a broad spectrum of diseases including
heart disease, cancer, neurodegenerative diseases, and the general aging process …