No matter how much you diet and hit the gym, muscle cells turn to fat as the body ages. Toned bods inevitably become flabby. Blame it on the cilia.

New research shows the tiny cellular antennae plays a key role in the muscle-to-fat transformation process. While the realization is unlikely to unlock the fountain of youth, it could help scientists develop new types of regenerative therapies.

The growing amounts of fat cells interspersed with muscle cells helps explain why humans become weaker as they age.

"The frailty of age is a huge biomedical problem," Dr. Jeremy Reiter, a professor of biochemistry and biophysics at the University of California, San Francisco, said in a news release. "This study helps pave the way to learn how muscles normally age, and provides a new way to possibly improve muscle repair."

Until recently, cilia were mostly ignored by researchers. Most scientists believed the tiny tentacle-like appendages extending from the surface of cells served no real function. Over the last decades, scientists have been taking a closer look at primary cilia.

The rigid appendages are found on the surfaces of all types of cells, and the latest research suggests they act like antennae, sensing and translating all kinds of observational data -- light, temperature, salinity, gravity. The cilia's transmission abilities are used by a variety of cell-signaling pathways.

In a previous study, UCSF researchers found injured muscles tend to generate a large number of fibro/adipogenic progenitors, or FAPs, fat-forming cells that live alongside muscle cells. These fat cells are more likely to host primary cilia.

Researchers hypothesized cilia play an important role in the formation of fat cells.

In the latest experiments, researchers tested their hypothesis by studying muscle injuries in mouse models in which scientists blocked the ability of FAPs to form cilia. Researchers measured lower concentrations of fat cells in the mouse models. Mice with both acute muscle injuries and chronic muscle injuries showed greater rates of muscle generation when less cilia were formed.

Simply by blocking the formation of cilia on FAPs, researchers were able to heal the muscles of a mouse with Duchenne muscular dystrophy.

Further analysis showed cilia-free FAPs triggered a so-called hedgehog signaling pathway, a pathway key to cell formation and generation. The pathway encouraged a higher muscle-to-fat ratio in mouse muscle. Scientists determined that the protein TIMP3 was key in this process, and were able to trigger the fat-killing pathway using batimastat, a molecule that mimics the effects of TIMP3.

"Now for the first time we have a handle on the cell type that turns muscle into fat, and we have a handle on the signaling pathway that controls the conversion," said Daniel Kopinke, a postdoctoral fellow in the Reiter lab. "Maybe one day we could use this knowledge to improve muscle function."

Researchers detailed their latest findings this week in the journal Cell.

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