Erica Clinkenbeard
Indiana University-Purdue University-Indianapolis, IN·Physiology
People with chronic kidney disease (CKD) often develop fragile bones, part of a condition called CKD mineral and bone disorder (CKD-MBD). Fractures in these patients are linked to higher death rates.
- Fields
Physiology
Medicine & Clinical Research
Biochemistry
- Topics
chronic kidney disease
mineral and bone disorder
bone loss
- Grants
- 1 known grant, through Nov 2026
What they work on
- Test whether low iron weakens bone formation in CKD by reducing spermine, by giving spermine during iron deficiency to cultured bone-building cells (osteoblasts) and to mice with adenine diet-induced kidney failure.
- Determine whether genetically increasing spermine synthase, the enzyme that makes spermine, protects bone in iron-deficient mice with kidney failure.
- Use epigenetic sequencing to map how iron deficiency and polyamines change DNA accessibility, and through it gene expression, in osteoblasts.
- Test whether iron deficiency in CKD speeds polyamine breakdown, by genetically or pharmacologically blocking the breakdown enzymes spermine oxidase and N-acetyltransferase in mice.
More about the research
Poor bone upkeep also releases calcium and phosphorus into the blood, which can contribute to hardened, calcified blood vessels. Many CKD patients also have iron-deficiency anemia, but it is unclear how low iron directly affects bone. Iron deficiency is known to blunt bone formation. It also lowers cell levels of spermine and spermidine, small molecules called polyamines that osteoblasts (bone-building cells) need to mature and work. CKD patients also have lower spermine levels.
Why it matters
Fragile bones and fractures are a serious and deadly problem for people with chronic kidney disease, and iron-deficiency anemia is common in these patients. If low iron weakens bone by depleting polyamines such as spermine, then polyamine supplementation or blocking polyamine-degrading enzymes could become new treatment targets. Such approaches could protect bone and inform how iron deficiency is managed in CKD patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Demetrios Braddock
Yale University, CT·Medicine & Clinical Research
Identify the signaling pathways by which ENPP1, the only human enzyme that makes the mineral inhibitor pyrophosphate, regulates bone mass, including pathways independent of its enzyme activity.
Fernando Fierro
University of California-Davis, CA·Physiology
Uncover how spermine synthase (SMS) deficiency impairs bone mineralization, testing whether excess spermidine blocks hypusination, the chemical activation of the protein eIF5A, and disrupts mitochondrial release of calcium phosphate.
Nicolae David
Northwestern University, IL·Physiology
Test whether inflammation suppresses HNF4α, a gene-activating transcription factor, in bone-forming osteoblasts, creating a feed-forward loop that blunts parathyroid hormone (PTH) response, by switching Hnf4α2 on or off in mice with CKD or PTH challenges.
The school
Indiana University-Purdue University-Indianapolis: 25 labs on PI Pages, $89M a year on research, 120 research doctorates a year.
More about Indiana University-Purdue University-Indianapolis
Reach out
A start for your email. Fill in the brackets.