Environmental Factor, January 2011, National Institute of Environmental Health Sciences
NIEHS to fund new mitochondrial dysfunction studies
By Eddy Ball
NIEHS issued a new funding opportunity announcement (FOA)(https://grants.nih.gov/grants/guide/rfa-files/RFA-ES-11-007.html) Nov. 30 for projects to identify biomarkers for early detection of environmentally induced mitochondrial dysfunction. Applications will be accepted from Jan. 3 through Feb. 3.
Mitochondrial dysfunction results in deficits in cellular bioenergy production and is associated with numerous chronic diseases. It also may reflect, in part, the vulnerability of mitochondria to environmental influences.
NIEHS has committed $2.5 million this year to fund between six and eight research projects to seek new markers of early mitochondrial dysfunction that results from environmental exposures or stressors.
According to the announcement, the new grant opportunity will stimulate the development of biomarkers of mitochondrial dysfunction in easily accessible tissues, including blood, buccal mucosa, and urine, by enhancing the basic understanding of how environmental stressors affect mitochondrial function. The new NIEHS grants will help investigators explore several important areas:
- Enhancing the understanding of how the more severe effects on mitochondrial function in target tissues relate to milder effects in surrogate tissues
- Understanding whether alterations in mitochondrial endpoints are adaptive or adverse - transient or persistent - effects
- Determining which endpoints signal early effects on mitochondrial function before more severe tissue phenotypes are apparent
NIEHS intends the funding to encourage development of biomarkers of mitochondrial dysfunction, using animal models and other experimental models that can help to identify environmental stressors that inhibit normal mitochondrial function. These models will then enable the development of approaches and candidate markers to serve as the basis for discovering biomarkers of early mitochondrial dysfunction in human population studies linking exposure to disease.
The new funding of mitochondrial biomarker research could help address some of the questions surrounding human diseases and help establish tools for further research to answer lingering questions about the role of the environment in mitochondrial dysfunction, both clinical and subclinical, in a range of conditions including autism (see related story (https://factor.niehs.nih.gov/2011/january/science-mitochondrial.cfm)).
Scientific Review Administrator Leroy Worth, Ph.D.(mailto:email@example.com), is serving as peer review contact on the FOA, and Program Administrator Dan Shaughnessy, Ph.D.(mailto:firstname.lastname@example.org), is providing scientific and research support.