Transient receptor potential (TRP) channels are ubiquitously expressed
cellular sensors that respond to changes in the cellular environment. They act in
nociception, taste perception, thermosensation, mechanosensing, osmolarity sensing,
and signal transduction. Mammalian TRP channels comprise 28 members divided into
six subfamilies: TRPA (ankyrin), TRPC (canonical), TRPM (melastatin), TRPML
(mucolipin), TRPP (polycystin) and TRPV (vanilloid). TRP mutations that result in
either gain or loss of function have been linked to several human diseases, among them
hypertension, cardiac hypertrophy, obesity, and diabetes. In the myocardium, TRP
channels modulate Ca+2 handling and are differentially expressed in models of cardiac
remodeling and dysfunction. TRP channels are also involved in insulin release from
pancreatic beta-cells and glucose tolerance in rodent models of type 2 diabetes. Some
of these channels promote thermogenesis and thus prevent diet-induced obesity. How
TRP channels are modulated in vivo is still unknown since few endogenous ligands
were identified so far. However, a wide range of natural products with therapeutic
potential activates TRP channels and might serve as models for new drug discovery
and development to prevent cardiometabolic morbidity and mortality. Studies with
TRP channels show promising results, but the translation to preventive or therapeutic
strategies against cardiometabolic diseases is challenging since they are found in
multiple tissues and enrolled in several physiological actions, which increases the risk
of adverse effects.
Keywords: Adipose tissue, Cardiovascular diseases, Cardiometabolic syndrome,
Heart, Obesity, Pancreas, Type 2 diabetes, Transient receptor potential channels,
TRPA1, TRPC, TRPM, TRPV.
