individuals having a normal weight [45]. This can be because the reactive oxygen species (ROS) tion by OA chondrocytes stems in the mechanical overload with the joints, which further production by OA chondrocytes stems from the mechanical overload of the joints, which amplifies cartilage degradation [10,46]. Thus, OA is typically created in weight-bearfurther amplifies cartilage degradation [10,46]. For that reason, OA is generally developed in weighting joints and is mostly observed within the decreasing order of the knee, hip, and hand [33]. bearing joints and is mainly observed in the decreasing order on the knee, hip, and hand [33].Figure three. Structural image of typical and OA-diagnosed joints. OA primarily impacts the cartilage, Figure three. Structural image of normal and OA-diagnosed joints. seem in OA-diagnosed joints are bone, and synovial membrane. Some prevalent symptoms that OA mostly impacts the cartilage, bone, and synovial membrane. Some prevalent symptoms that seem in OA-diagnosed joints are shown above. shown above.four. iPSC Illness Modeling four. iPSC Disease Modeling drastically expanded our expertise of pathology by recapitulating Disease modeling has the Disease modelingand etiology expanded our expertise of pathologydecades, animals pathophysiology has greatly of different human illnesses [47,48]. For by recapitulating the served as the most typical experimental models of disease prior to decades,trials have pathophysiology and etiology of many human ailments [47,48]. For human animalsperformed [47]. Nonetheless, the limitations on account of interspecies variations have led are have served because the most common experimental models of illness before human trials are performed [47]. Nevertheless, the limitations because of interspecies differencesHence, to high rates of translation failure amongst human and animal models [47,49]. have led to high ratesdisease model utilizing human iPSCs (hiPSCs)animal models [47,49]. Hence, constructing a of translation failure among human and became lucrative in 2008 when Park et al. were in a position to create disease-specific iPSCs from patients diagnosed with constructing a disease model making use of human iPSCs (hiPSCs) became lucrative in 2008 when genetic ailments (Parkinson’s disease-specific iPSCs illness, Gaucher illness form III, Park et al. were capable to generatedisease, Huntington’s from individuals diagnosed with geetc.) [47,48,50,51]. By establishing a customized disease model illness somatic cells netic illnesses (Parkinson’s illness, Huntington’s illness, Gaucherusing thetype III, and so forth.) from every single patient, iPSC modeling can precisely detect any utilizing negative effects cells from [47,48,50,51]. By establishing a personalized disease modeladversethe somatic of prospective therapies iPSC modeling can precisely detect of disease phenotypes of prospective every single patient,and provide a far better understandingany adverse side effects[47,50,51]. treatment options Recent advancements have significantly improved the efficacy and applicability of and provide a far better understanding of disease phenotypes [47,50,51]. iPSC illness modeling. Most notably, Volpato and Webber have recommended new tactics to lower any genetic variations by getting homogeneous cellular composition and establishing controls utilizing stem cell banks [52]. Additionally, advancements in threedimensional organoids, microfluidic organ chips, and Nisoxetine Monoamine Transporter bioprinting (that will be discussed later) have opened new doors for iPSC illness modeling beyond the previous two-dimensional co-culturing [50].Cell