Serotonin regulation of mitochondria in kidney diseases.

Serotonin, while conventionally recognized as a neurotransmitter in the CNS, has recently gained attention for its role in the kidney. Specifically, serotonin is not only synthesized in the kidney, but it also regulates glomerular function, vascular resistance, and mitochondrial homeostasis. Because of serotonin's importance to mitochondrial health, this review is focused on the role of serotonin and its receptors in mitochondrial function in the context of acute kidney injury, chronic kidney disease, and diabetic kidney disease, all of which are characterized by mitochondrial dysfunction and none of which has approved pharmacological treatments.

Mitophagy regulates mitochondrial number following pharmacological induction of mitochondrial biogenesis in renal proximal tubule cells.

Mitochondrial biogenesis (MB) induction through the activation of the 5-Hydroxytriptamine (5-HT) 1F receptor (HTR1F) is a promising mechanism for the treatment of diseases characterized by mitochondrial dysfunction, such as acute kidney injury (AKI). While several studies report pharmacological activation of MB in the proximal tubule, it is unclear how the proximal tubule regulates itself once the pharmacological activation is removed. Mitophagy is the process of selective mitochondria degradation.

Lasmiditan restores mitochondrial quality control mechanisms and accelerates renal recovery after ischemia-reperfusion injury.

Background: Mitochondrial dysfunction is a well-established result of acute kidney injury (AKI). Previously, we identified that 5-hydroxytryptamine 1F (5-HT) receptor agonism with lasmiditan induces mitochondrial biogenesis (MB) and improves renal vasculature and function in an AKI mouse model. We hypothesize that lasmiditan also modulates mitochondrial dynamics and mitophagy in a mouse model of AKI.

Lasmiditan promotes recovery from acute kidney injury through induction of mitochondrial biogenesis.

Acute kidney injury (AKI) involves rapid loss of renal function and occurs in 8-16% of hospitalized patients. AKI can be induced by drugs, sepsis, and ischemia-reperfusion (I/R). Hallmarks of AKI include mitochondrial and microvasculature dysfunction as well as renal tubular injury.

A Quantitative Assessment of Staphylococcus aureus Community Carriage in Yuma, Arizona.

Background: Disease control relies on pathogen identification and understanding reservoirs. Staphylococcus aureus infection prevention is based upon decades of research on colonization and infection, but diminishing returns from mitigation efforts suggest significant knowledge gaps. Existing knowledge and mitigation protocols are founded upon culture-based detection, with almost no information about pathogen quantities.

Health Disparities in Staphylococcus aureus Transmission and Carriage in a Border Region of the United States Based on Cultural Differences in Social Relationships: Protocol for a Survey Study.

Background: Health care-associated Staphylococcus aureus infections are declining but remain common. Conversely, rates of community-associated infections have not decreased because of the inadequacy of public health mechanisms to control transmission in a community setting. Our long-term goal is to use risk-based information from empirical socio-cultural-biological evidence of carriage and transmission to inform intervention strategies that reduce S aureus transmission in the community.