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32 %u010ceskoslovensk%u00e1 fyziologie 73/2025 %u010d. 2P%u0158EHLEDN%u00c9 %u010cL%u00c1NKYInterakce kostern%u00edch sval%u016f a jater p%u0159i steatotick%u00e9m onemocn%u011bn%u00ed jater spojen%u00e9m s metabolickou dysfunkc%u00edInteraction of skeletal muscles and liver in metabolic dysfunction-associated steatotic liver disease Ahmed Mohamed Abdelhamid Ibrahim, Tumisang Edward Maseko, Zuzana %u010cervinkov%u00e1, Moustafa ElkalafUnivezita Karlova, L%u00e9ka%u0159sk%u00e1 fakulta v Hradci Kr%u00e1lov%u00e9, Fyziologick%u00fd %u00fastav, Hradec Kr%u00e1lov%u00e9SOUHRNSteatotick%u00e9 onemocn%u011bn%u00ed jater spojen%u00e9 s metabolickou dysfunkc%u00ed (MASLD) je ned%u00e1vno p%u0159ijat%u00e1 terminologie pro nealkoholovou tukovou chorobu jater (NAFLD), kter%u00e1 klade d%u016fraz na dal%u0161%u00ed metabolick%u00e1 rizika a posti%u017een%u00ed extrahepat%u00e1ln%u00edch tk%u00e1n%u00ed; MASLD je velmi %u010dast%u00e9 onemocn%u011bn%u00ed u pacient%u016f s metabolick%u00fdmi komorbiditami, jako je diabetes mellitus 2. typu, a je v%u00fdznamn%u011b spojeno s dysfunkc%u00ed kostern%u00edho svalstva. Tyto dv%u011b tk%u00e1n%u011b se b%u011bhem progrese onemocn%u011bn%u00ed vz%u00e1jemn%u011b ovliv%u0148uj%u00ed bu%u010f p%u0159%u00edmou metabolickou interakc%u00ed, spole%u010dn%u00fdmi patofyziologick%u00fdmi mechanismy, nebo vz%u00e1jemn%u00fdm p%u016fsoben%u00edm sign%u00e1ln%u00edch modul%u00e1tor%u016f, jako jsou hepatokiny a myokiny. %u00dadaje o t%u00e9to interakci v%u011bt%u0161inou dokumentovaly negativn%u00ed dopad t%u011bchto sign%u00e1ln%u00edch molekul, nicm%u00e9n%u011b poskytly nov%u00e9 poznatky pro pochopen%u00ed komplexnosti onemocn%u011bn%u00ed, kter%u00e9 nesouvis%u00ed pouze se stravou, jak prok%u00e1zaly studie proveden%u00e9 na %u0161t%u00edhl%u00fdch pacientech s diagn%u00f3zou MASLD. Tento p%u0159ehled popisuje interakci mezi jatern%u00ed a svalovou tk%u00e1n%u00ed s c%u00edlem l%u00e9pe porozum%u011bt komunikaci mezi ob%u011bma tk%u00e1n%u011bmi a zd%u016fraz%u0148uje nov%u00e9 terapeutick%u00e9 strategie navr%u017een%u00e9 pro l%u00e9%u010dbu a %u00fa%u010dinn%u00e9 zvl%u00e1d%u00e1n%u00ed MASLD a jej%u00edch komplikac%u00ed.Kl%u00ed%u010dov%u00e1 slova: MASLD, NAFLD, myokiny, hepatokiny, sign%u00e1ln%u00ed molekulySUMMARYMetabolic dysfunction-associated steatotic liver disease (MASLD) is a recently adopted terminology for non-alcoholic fatty liver disease (NAFLD), to emphasize the metabolic risks and dysfunction of non-hepatic tissues. MASLD is a highly prevalent disease amongst patients with metabolic comorbidities such as type 2 diabetes mellitus and is strongly associated with skeletal muscle dysfunction. Skeletal muscle and liver tissue reciprocally influence each other via direct metabolic interplay, shared pathophysiological mechanisms and crosstalk of signalling modulators such as hepatokines and myokines. Reports of such interactions mostly documented the negative impact of these signalling molecules, nevertheless, they provided new insights in understanding the complexity of the disease, which is not solely related to the diet as proved by studies performed on lean patients diagnosed with MASLD. This review demonstrates the hepatic-muscular interaction aiming for a better understanding of the communication between both tissues and emphasizes the novel therapeutic strategies proposed for the treatment and productive management of MASLD and its complications. Keywords: MASLD, NAFLD, myokines, hepatokines, signalling molecules INTRODUCTIONAnalysing the mutual relationship between hepatic and skeletal muscle tissue during MASLD progression stems from proper understanding of the complex pathophysiological pathways associated with the disease. Thorough research in this field deduced that the pathogenesis originates from the complex interplay between metabolic diseases and conditions such as insulin resistance and type 2 diabetes mellitus (T2DM) (Ziolkowska et al., 2021). This subsequently leads to the accumulation of excess amounts of fat in hepatocytes resulting in oxidative stress and generation of reactive oxygen species (Li & Wang, 2020). The inflammatory and stress-based changes lead to defects in the mitochondria which spans from morphological defect, compromised mitochondrial membrane permeability, to alterations in the mitochondrial DNA. Eventually, this leads to the malfunctioning of skeletal muscle tissue. A more direct communicative nature between hepatic and skeletal muscle tissue is observed through investigating the role of signalling modulators expressed by both tissues and how their imbalances could lead to a range of pathological changes in the reciprocate organ. A relevant example is fetuin-A, a carrier protein made in the liver that has an adverse effect on skeletal muscles by inducing insulin resistance as well as influencing systemic inflammation (Keating et al., 2023). Signalling molecules arising from skeletal muscles such as myokines also play a crucial role in MASLD. For instance, the myokine myostatin, which is highly secreted in obesity and MASLD, negatively regulates muscle growth leading to sarcopenia (Merli et al., 2015). Adipokines such as leptin and adiponectin are signalling modulators arising from adipose tissue that also facilitate the crosstalk among the liver, skeletal muscle, and adipose tissue, establishing the muscle-liver-fat signalling axis. Leptin regulates physiological lipid metabolism and energy balance, and its dysregulation in MASLD has an eminent negative impact on hepatic and skeletal muscle tissue (Li & Wang, 2020). Novel research studies demonstrate the positive influence of exercise on decreasing the amount of oxidative stress and endoplasmic