A primer for Fibroblast Growth Factor 16 (FGF16).

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

During the discovery of the Fibroblast Growth Factor superfamily, scientists were determined to uncover all the genes that encoded FGF proteins. In 1998, FGF16 was discovered with classical cloning techniques in human and rat heart samples. FGF16 loss- and gain-of-function experiments in several organisms demonstrated a conserved function in vertebrates, and as a component of the FGF9 subfamily of ligands (FGF-E/-9/-20), is functionally conserved and sufficient to rescue loss-of-function phenotypes in invertebrates, like C. elegans. FGF16 has a broad expression pattern, predominantly expressed in brown adipose tissue, heart, with low but detectable levels in the brain, olfactory bulb, inner ear, muscle, thymus, pancreas, spleen, stomach, small intestine, and gonads (testis and ovary). FGF16 is also expressed moderately in the late developing limb bud. Despite its expression levels, this ligand plays notable roles in autopod metacarpal development; loss of one allele causes congenital metacarpal 4-5 fusion and hand deformities in humans. The broad expression pattern of FGF16 in several tissues underscores its multifaceted roles in stem cell maintenance, proliferation, cell fate specification, and metabolism.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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