Acute kidney injury (AKI) is defined as a pathological condition in which the glomerular filtration rate decreases rapidly over a short period of time, resulting in changes in the physiological function and tissue structure of the kidney. An increasing amount of evidence indicates that there is an inseparable relationship between acute kidney injury and chronic kidney disease (CKD). With the progress in research in this area, researchers have found that the recovery of AKI may also result in the occurrence of CKD due to its own maladaptation and other potential mechanisms, which involve endothelial cell injury, inflammatory reactions, progression to fibrosis and other pathways that promote the progress of the disease. Based on these findings, this review summarizes the occurrence and potential mechanisms of maladaptive repair in the progression of AKI to CKD and explores possible treatment strategies in this process so as to provide a reference for the inhibition of the progression of AKI to CKD.

Plaque rupture in atherosclerosis (AS) is a major cause of acute cardiovascular events. Macrophage-induced inflammatory responses and accumulation of excess reactive oxygen species (ROS) primarily induce unstable plaques. Therefore, targeting ROS clearance and functional modulation of macrophages are clinically crucial for improving plaque stability and inhibiting AS progression. Here, we constructed a bionic nano-delivery platform, PBP@siR@PM, using platelet membranes (PM) coated with black phosphorus nanosheets (BPNSs) to target macrophages in atherosclerotic plaques. Meanwhile, PM-coated BPNSs (PBP@siR@PM) were used to deliver small interfering RNA silencing Ca²⁺/calmodulin-dependent protein kinase γ (CaMKIIγ) into macrophages. Furthermore, macrophage efferocytosis was restored by inhibiting CaMKIIγ and increasing the expression of MerTK, a cytosolic receptor, thus promoting the clearance of apoptotic cells from plaques. This study demonstrated that intraplaque macrophage-targeted therapy using the bionic nano-delivery platform PBP@siR@PM effectively removed excess ROS from macrophages, promoted efferocytosis, cleared apoptotic cells in plaques, improved plaque stability, and largely inhibited AS progression in ApoE^-/- mice after high fat diet. In summary, this study proposes a therapeutic strategy for AS and highlights the outstanding therapeutic potential of biomimetic nanomaterials in this type of chronic inflammatory disease. STATEMENT OF SIGNIFICANCE: Rupture of atherosclerotic unstable plaques is a major cause of acute cardiovascular events. Macrophage-induced chronic inflammation and oxidative stress due to overloaded ROS are major contributors to plaque rupture. In this study, we focused on the improvement of macrophage efferocytosis within the plaque for the effective treatment of atherosclerosis. A bionic nano-delivery platform was constructed using platelet membranes (PM) coated black phosphorus nanosheets (BPNSs) to target macrophages in atherosclerotic plaques. In conclusion, intraplaque macrophage-targeted therapy based on the bionic nano-delivery platform PBP@siR@PM effectively scavenges overloaded ROS in macrophages, promotes efferocytosis, removes apoptotic cells from plaques, and improves plaque stability, which significantly inhibits the progression of atherosclerosis in ApoE^-/- mice after a high-fat diet.

Diabetic nephropathy and diabetic atherosclerosis often develop together and share similar metabolic disturbances. Lipid abnormalities are common in diabetes, yet their roles in kidney and vascular injury are not fully understood. In diabetic kidney disease, altered lipid uptake, reduced fatty acid oxidation, and accumulation of harmful lipid species contribute to cellular stress, mitochondrial injury, inflammation, and fibrosis. In parallel, disordered lipid handling in the vasculature promotes endothelial dysfunction and atherosclerotic plaque development. However, not all lipid accumulation appears to be detrimental, and some findings suggest adaptive or context-dependent effects, leading to inconsistent results across studies. In this review, we summarize current evidence on lipid metabolism in diabetic nephropathy and atherosclerosis, compare shared and distinct features, and discuss ongoing controversies. We also briefly address the therapeutic relevance of targeting lipid pathways and highlight areas that require further investigation. Compared with prior reviews that mainly discussed fatty kidney as an emerging concept in chronic kidney disease research, this review specifically focuses on diabetic kidney disease and integrates kidney-specific lipid trafficking, kidney–vessel crosstalk, conflicting evidence, and mechanism-based therapeutic implications.

Kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), and end-stage renal disease (ESRD), represent an interconnected clinical continuum characterized by complex etiologies, pathological heterogeneity, dispersed pathogenic cells, and limited therapeutic windows. Although current therapies can delay disease progression, they remain insufficient for precise renal lesion targeting, cell-specific intervention, and coordinated regulation of oxidative stress, inflammation, cell death, immune imbalance, microvascular injury, and fibrosis. Biomimetic nanomedicine has recently emerged as a promising preclinical strategy by mimicking natural biological structures, optimizing biointerfaces, and enhancing selective intrarenal delivery. Compared with conventional nanocarriers, biomimetic nanoplatforms based on cell membrane camouflage, engineered extracellular vesicles, extracellular matrix mimicry, ligand-guided delivery, and nanozyme catalysis can improve circulation stability, lesion recognition, and multipathway therapeutic regulation. In this review, we systematically summarize biomimetic nanomedicine strategies across AKI-, CKD-, and ESRD-related settings, focusing on cell membrane-coated nanoparticles, targeting ligand modification, biomimetic nanozymes, engineered extracellular vesicles, and extracellular matrix-inspired systems. We also discuss their expanded applications in dialysis membrane engineering, transplant monitoring, and regenerative medicine. Finally, we analyze key translational challenges, including long-term biosafety, interspecies differences, protein corona effects, manufacturing scale-up, quality control, and regulatory translation. Although still mainly at the preclinical stage, biomimetic nanomedicine offers important potential for improving renal delivery efficiency, enhancing cellular selectivity, and enabling synergistic intervention in kidney diseases.

Chronic stress is a pervasive psychophysiological burden and an independent risk factor for chronic kidney disease (CKD). Large-scale cohort studies confirm that stress exposure significantly increases CKD risk and accelerates renal decline, even after adjusting for traditional confounders. However, the neuroendocrine mechanisms translating stress into direct kidney damage remain unclear. This review focuses on the brain–kidney axis, a bidirectional framework integrating neural, endocrine, and immune signals. Under chronic stress, sustained overactivation of the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS), coupled with secondary renin–angiotensin–aldosterone system (RAAS) dysregulation, creates a deleterious intrarenal milieu. Unlike classical models driven by high salt or metabolic disorders, a proposed hallmark of stress-induced injury is the non-classical activation of the mineralocorticoid receptor (MR). Given MR’s equal affinity for cortisol and aldosterone, the protective barrier maintained by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is compromised under persistent glucocorticoid elevation. This may allow cortisol to escape inactivation and aberrantly activate intrarenal MR, a process putatively termed gluco-mineralo cross-activation. This mechanism is hypothesized to initiate profibrotic cascades via NADPH oxidase 4 (NOX4)/ROS/TGF-β/Smad pathways and amplifies the complement C5a-C5a receptor 1 inflammatory axis, culminating in fibrosis and sclerosis. Based on these insights, we propose stress-related kidney disease (SRKD) as a distinct clinical entity. This review synthesizes current evidence to guide precision interventions targeting the brain–kidney axis.