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However, under prolonged and abnormal loading conditions, the remodeling processes can become maladaptive, leading to altered physiological function and the development of pathological cardiac hypertrophy and heart failure. Although the mechanisms underlying mechanotransduction are far from being fully elucidated, human and mouse genetic studies have highlighted various cytoskeletal and sarcolemmal structures in cardiac myocytes as the likely candidates for load transducers, based on their link to signaling molecules and architectural components important in disease pathogenesis. In this review, we summarize recent developments that have uncovered specific protein complexes linked to mechanotransduction and mechanotransmission within the sarcomere,\n            <jats:sup>\n              <jats:xref ref-type=\"bibr\"\/>\n            <\/jats:sup>\n            the intercalated disc,\n            <jats:sup>\n              <jats:xref ref-type=\"bibr\"\/>\n            <\/jats:sup>\n            and at the sarcolemma.\n            <jats:sup>\n              <jats:xref ref-type=\"bibr\"\/>\n            <\/jats:sup>\n            The protein structures acting as mechanotransducers are the first step in the process that drives physiological and pathological cardiac hypertrophy and remodeling, as well as the transition to heart failure, and may provide better insights into mechanisms driving mechanotransduction-based diseases.\n          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