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Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.

Cardiac voltage-sensitive optical mapping records changes in transmembrane potential from cardiac tissue by staining the preparation with a voltage-sensitive dye and imaging fluorescence changes during electrical activation; the resulting optical action potentials can be used to map activation time, action potential duration, conduction velocity, wavefront propagation, and arrhythmia dynamics. The optical signal represents a relative fluorescence change from a tissue volume rather than a single-cell intracellular recording, so spatial resolution, sampling rate, voltage resolution, optical magnification, light penetration, and motion control must be considered together when interpreting optical action potentials.

Neuronal voltage-sensitive dye imaging detects membrane-potential-dependent optical changes from dyes associated with neuronal membranes, enabling optical recording of electrical activity from single neurons, dendrites, axons, spines, or neuronal populations in brain slices and cultured neurons. VSD signals are typically reported as fractional fluorescence or absorbance changes over baseline, such as ΔF/F or ΔI/I, and published protocols use high-speed cameras or photodiode arrays because neuronal voltage signals occur on millisecond time scales. Fast VSD imaging can be applied at two common scales: bulk staining of brain slices to measure circuit-level spatiotemporal activity, and single-cell loading or biolistic delivery to record membrane-potential transients from individual neuronal compartments. Optical signals should be interpreted as membrane-potential-related readouts, and validation by simultaneous electrophysiology or pharmacological controls is recommended when the experimen

Acute brain-slice whole-cell patch-clamp recording measures membrane voltage or ionic current from visually targeted cells in living brain slices; after giga-seal formation, the membrane under the pipette is ruptured to provide low-resistance electrical access to the cell interior, enabling current-clamp analysis of excitability and voltage-clamp analysis of synaptic or membrane currents. Acute slices preserve local tissue architecture better than dissociated preparations and allow visually guided recording from defined brain regions or fluorescently labeled cells; however, whole-cell access also permits exchange between pipette solution and cytoplasm, so intracellular dialysis must be considered when interpreting signaling-dependent phenomena.

Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.