ReviewAmerican journal of translational research2026
Micro Zhēngjiǎ as a reversible microstructural lesion network in diabetic myocardial fibrosis: mechanistic insights and therapeutic implications of Huoxue-Tongluo therapy.
Review in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Diabetic myocardial fibrosis (DMF) is a prominent pathological process that leads to the progression of diabetic heart disease, and yet the underlying mechanisms have not been properly clarified. Recently, a new paradigm called Micro Zhēngjiǎ lesion has been implicated, with microstructural changes in the myocardial capillaries being indicated as critical factors in the development of diabetic fibrosis. The purpose of the review is to investigate the mechanistic basis of the Micro Zhēngjiǎ lesion in DMF and its implications across tissue, cellular, and molecular levels. This article summarizes findings from histological and imaging studies, which show the structural and functional impairments of the myocardial extracellular space, as well as dysregulation of fibrosis-related signaling pathways, in the diabetic heart. Moreover, potential treatment interventions are reviewed, especially Huoxue-Tongluo therapy. This approach, which aims to activate blood circulation and dredge collaterals, combines traditional Chinese medicine with modern pharmacological principles to reverse the development of DMF. By targeting major inflammatory mediators, improving microcirculation, and regulating fibroblast activation, Huoxue-Tongluo therapy has the potential to be used as an alternative or complementary approach to conventional therapy. The review proves the translational potential of the given therapeutic paradigm and suggests future research directions to investigate the multifaceted interplay of microstructural lesions, metabolic dysfunction, and fibrosis in the diabetic heart in depth.
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