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Guo Huang

University of California-San Francisco, CA·Physiology

After a heart attack, adult humans cannot replace the heart muscle cells they lose. Over time this leads to heart failure.

Fields

Physiology

Biology

Genetics

Topics

heart regeneration

cardiac regeneration

cardiomyocyte proliferation

Grants
2 known grants, through Feb 2027

What they work on

  1. Determine how Bcl6, a gene-regulating protein switched on after birth, controls heart muscle cell division during heart growth and repair after injury, using heart-specific Bcl6 deletion in mice.
  2. Test the role of a likely direct Bcl6 target gene in stopping heart cell division, using genetic rescue experiments in mice.
  3. Measure total heart muscle cell number accurately by making whole mouse hearts transparent, immunostaining them, and imaging them with light-sheet microscopy.
  4. Compare how Bcl6 is regulated across development and species, including mice and cold-blooded naked mole-rats, to see if it rose alongside warm-bloodedness.
  5. Test whether heat-producing tissues drive heart cell division arrest after birth and limit repair after heart attack in adult mice, and identify the signals linking them to the heart.

More about the research

Adult zebrafish and newborn mice, by contrast, can regrow heart muscle by dividing their existing heart muscle cells, called cardiomyocytes. Mice lose this ability within a week of birth. The research here asks what switches regeneration off. Earlier work by the team suggested that becoming warm-blooded (endothermy) plays a part, through the heat-producing (thermogenic) signals that come with it, such as rising thyroid hormone and adrenergic signaling around birth. The two projects follow this idea down to specific genes and organs.

Why it matters

Heart failure is rising because adult hearts cannot replace muscle lost after a heart attack. By identifying the natural brakes on heart regeneration, such as Bcl6 and signals from heat-producing tissues, this work could suggest new targets and strategies to help the adult heart repair itself after injury.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Genetic circuitry governing heart growth and repair

NIH · Mar 2022 – Feb 2027

Molecular control of cardiac regenerative potential

NIH · Dec 2017 – Dec 2026

Closest labs

Malcolm Maden

University of Florida, FL·Biology

Determine whether the spiny mouse heart truly regenerates after a heart attack through cardiomyocyte division, using tissue staining for fibrosis, cell division and cell death, compared with lab mice.

Joseph Hill

University of Texas Southwestern Medical Center, TX·Medicine & Clinical Research

Determine how endothelial Fli1 protects the heart under ischemic stress, using tamoxifen-inducible mice that lack Fli1 only in blood vessel lining cells, and manipulate Fli1 activity in models of ischemic heart disease.

Jidong Fu

Ohio State University, OH·Medicine & Clinical Research

Characterize how Masir, a membrane-associated long noncoding RNA, protects heart muscle cells from ischemic injury by enhancing membrane repair, and assess its safety in mouse models.

The school

University of California-San Francisco: 89 labs on PI Pages, $2.1B a year on research, 164 research doctorates a year.

More about University of California-San Francisco

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