Background: Up to 80% of men and 50% of women will have androgenetic alopecia (AGA) at some point in their lives, making it the most prevalent kind of hair loss. As a result of the actions of dehydrotestosterone (DHT), a testosterone metabolite, on androgen-sensitive hair follicles, the width, length, and color of affected hair gradually decrease in AGA. The arrector pili muscle is made up of fusiform cells that don't have cytoplasmic striations and have centralized, cigar-shaped nuclei. These muscles round the hair follicle in the bulge area and are linked to it at an acute angle. Research has shown that the dermal sheath of hair follicles in both rats and humans contains alpha smooth muscle-actin (α-SMA), however this protein is not found in the dermal papilla cells. In this post, we will take a look at the pathophysiology of androgenic alopecia and how Alpha Smooth Muscle Actinin plays a part in it. The loss of structural integrity in hair follicles might be one way that α-SMA contributes to AGA. In the vertex area of AGA patients, the expression of α-SMA is significantly reduced. In addition, compared to the occipital area, the vertex region of AGA patients shows considerably decreased α-SMA expression.