Disclosed within is a mouse, and cells derived therefrom, which are homozygous for a disrupted δ-sarcoglycan gene, the disruption in said gene having been introduced into the mouse or an ancestor of the mouse at an embryonic stage. Said disruption prevents the synthesis of functional δ-sarcoglycan in cells of the mouse and results in the mouse having a reduced amount of β- and ε-sarcoglycan and sarcospan, and a disruption of the sarcoglycan-sarcospan complex in smooth muscle of the mouse. Said disruption also results in a reduced amount of sarcospan, α-, β-, γ-, and ε-sarcoglycan in the sarcolemma of skeletal and cardiac muscles of the mouse, compared to the amounts of said components in a mouse lacking disrupted δ-sarcoglycan genes. Preferred specific disruptions of the δ-sarcoglycan gene are listed. Also disclosed is a mouse, and cells derived therefrom, which are homozygous for a disrupted β-sarcoglycan gene, the disruption in said gene having been introduced into the mouse or an ancestor of the mouse at an embryonic stage. The disruption prevents the synthesis of functional β-sarcoglycan in cells of the mouse and results in the mouse having a reduced amount of δ- and ε-sarcoglycan and sarcospan and α-dystroglycan in smooth muscle of the mouse. The disruption also results in a disruption of the sarcoglycan-sarcospan complex in smooth muscle of the mouse, and a reduced amount of sarcospan, α, γ, δ- and ε-sarcoglycan in the sarcolemma of skeletal and cardiac muscles of the mouse, compared to the amounts of the components in a mouse lacking disrupted β-sarcoglycan genes. Preferred specific disruptions of the β-sarcoglycan gene are listed. A method for treating mammalian autosomal recessive limb-girdle muscular dystrophy type 2F in an individual is also disclosed. The method comprises, providing an expression vector which encodes a wild-type form of δ-sarcoglycan, and introducing the expression vector into skeletal and smooth muscle tissue of the individual under conditions appropriate for expression of the wild-type form of δ-sarcoglycan in said tissues. Examples of expression vectors for use in this method are adenovirus expression vector, a gutted adenovirus expression vector, and an adeno-associated expression vector. Also disclosed are methods for treating mammalian autosomal recessive limb-girdle muscular dystrophy type 2E, and type 2F, in an individual. The methods comprise, providing an expression vector which encodes a wild-type form of β-sarcoglycan, or δ-sarcoglycan, respectively, and introducing the expression vector into skeletal and smooth muscle tissue of the individual under conditions appropriate for expression of the wild-type form of the sarcoglycan gene in said tissues. The δ-sarcoglycan deficient, and β-sarcoglycan deficient mice of the present invention are useful in identifying therapeutic compounds for treatment of an individual diagnosed with δ-sarcoglycan-deficient limb-girdle muscular dystrophy, and β-sarcoglycan-deficient limb-girdle muscular dystrophy, respectively. A therapeutic method for treating ischemic heart disease caused by reduced expression of the sarcoglycan-sarcospan complex in vascular smooth muscle cells of an individual is also provided. The method comprises contacting the vascular smooth muscle cells of the individual with a vascular smooth muscle relaxant, such as Nicorandil. This method is also useful for preventing ischemic injury in skeletal and cardiac muscle of an individual caused by reduced expression of the sarcoglycan-sarcospan complex in the vascular smooth muscle cells of the individual. The method is also useful for treating mammalian autosomal recessive limb-girdle muscular dystrophy type 2F or type 2E in an individual. Other methods provided include a method for identifying a therapeutic compound for the treatment of ischemic heart disease in an individual caused by reduced expression of the sarcoglycan-sarcospan complex in the vascular smooth muscle cells of the individual, and also a method for identifying a therapeutic compound for the prevention of ischemic injury in skeletal and cardiac muscle of an individual which is caused by reduced expression of the sarcoglycan-sarcospan complex in vascular smooth muscle cells of the individual.