Platinum-perovskite nanocomposite-based Exosensor for specific detection of prostate cancer in clinical settings.

Exosomes, extracellular vesicles (EVs) with an average size of 50-150 nm, transfer various biomolecules and exchange signaling molecules between cells in a paracrine manner. Molecular investigations have revealed that EVs can reflect real-time metabolic changes in normal- and cancer-origin cells and thus harbor valid diagnostic biomarkers. Despite these advantages, the detection of low concentrations of cancer cell EVs in biological fluids is still a great challenge. Here, a new electrochemical Exosensor based on platinum-perovskite is developed for the direct detection of EVs using a biotinylated monoclonal CD63 antibody as a capture element. The label-free method exhibited higher sensitivity with a lower limit of quantification of 2000 EVs/µL with a dynamic linear range (LDR) of 2000 to 14,000 EVs/µL compared with other available methods. To enhance the selectivity of detection, EVs were simultaneously sandwiched between secondary antibodies of PSA (prostate-specific antigen), as an FDA-approved prostate cancer biomarker. Data indicated that this Exosensor can distinguish normal and cancer EVs in samples from healthy individuals and prostate cancer patients. Taken together, this technology offers a unique approach to label-free quantification of EVs and cancer detection in the early stages.

Plastic particle impacts on the cardiovascular system and angiogenesis potential.

The extensive application of plastics in different sectors such as packaging, building, textiles, consumer products, and several industries has increased in recent years. Emerging data have confirmed that plastic wastes and segregates are problematic issues in aquatic and terrestrial ecosystems. The decomposition of plastic particles (PPs) leads to the release of microplastics (MPs) and nanoplastics (NPs) into the surrounding environment and entry of these particles will be problematic in unicellular and multicellular creatures. It was suggested that PPs can easily cross all biological barriers and reach different organs, especially the cardiovascular system, with the potential to modulate several molecular pathways. It is postulated that the direct interaction of PPs with cellular and subcellular components induces genotoxicity and cytotoxicity within the cardiovascular system. Meanwhile, being inert carriers, PPs can intensify the toxicity of other contaminants inside the cardiovascular system. Here, in this review article, several underlying mechanisms related to PP toxicity in the cardiovascular system were discussed in detail.

Tumoroids, a valid preclinical screening platform for monitoring cancer angiogenesis.

In recent years, biologists and clinicians have witnessed prominent advances in in vitro 3D culture techniques related to biomimetic human/animal tissue analogs. Numerous data have confirmed that unicellular and multicellular (tumoroids) tumor spheroids with dense native cells in certain matrices are sensitive and valid analytical tools for drug screening, cancer cell dynamic growth, behavior, etc. in laboratory settings. Angiogenesis/vascularization is a very critical biological phenomenon to support oxygen and nutrients to tumor cells within the deep layer of solid masses. It has been shown that endothelial cell (EC)-incorporated or -free spheroid/tumoroid systems provide a relatively reliable biological platform for monitoring the formation of nascent blood vessels in micron/micrometer scales. Besides, the paracrine angiogenic activity of cells within the spheroid/tumoroid systems can be monitored after being treated with different therapeutic approaches. Here, we aimed to collect recent advances and findings related to the monitoring of cancer angiogenesis using unicellular and multicellular tumor spheroids. Vascularized spheroids/tumoroids can help us in the elucidation of mechanisms related to cancer formation, development, and metastasis by monitoring the main influencing factors.

Discovery of a Novel Dual Targeting Peptide for Human Glioma: From In Silico Simulation to Acting as Targeting Ligand.

Purpose: Receptor-mediated transcytosis (RMT) is a more specific, highly efficient, and reliable approach to crossing the blood-brain-barrier (BBB) and releasing the therapeutic cargos into the brain parenchyma. Methods: Here, we introduced and characterized a human/mouse-specific novel leptin-derived peptide using in silico, in vitro and in vivo experiments. Results: Based on the bioinformatics analysis and molecular dynamics (MD) simulation, a 14 amino acid peptide sequence (LDP 14) was introduced and its interaction with leptin-receptor (ObR) was analyzed in comparison with an well known leptin-derived peptide, Lep 30. MD simulation data revealed a significant stable interaction between ligand binding domains (LBD) of ObR with LDP 14. Analyses demonstrated suitable cellular uptake of LDP 14 alone and its derivatives (LDP 14-modified G4 PAMAM dendrimer and LDP 14-modified G4 PAMAM/pEGFP-N1 plasmid complexes) via ObR, energy and species dependent manner (preferred uptake by human/mouse cell lines compared to rat cell line). Importantly, our findings illustrated that the entry of LDP 14-modified dendrimers in hBCEC-D3 cells not only is not affected by protein corona (PC) formation, as the main reason for diminishing the cellular uptake, but also PC per se can enhance uptake rate. Finally, fluorescein labeled LDP 14-modified G4 PAMAM dendrimers efficiently accumulated in the mice brain with lower biodistribution in other organs, in our in vivo study. Conclusion: LDP 14 introduced as a novel and highly efficient ligand, which can be used for drugs/genes delivery to brain tissue in different central nervous system (CNS) disorders.

Xenogeneic Transplantation Promoted Human Exosome Sequestration in Rat Specific Organs.

Purpose: Here, we aimed to study the distribution pattern of normal and cancer xenogeneic exosomes (Exos) and possible interspecies reactions in a rat model. Methods: Exos were isolated from normal Human umbilical vein endothelial cells (HUVECs) and MDA-MB-231 breast cancer cells. Diameter size and zeta potential distribution were studied using dynamic light scattering (DLS). The morphology of isolated Exos was monitored by scanning electron microscopy (SEM) images. Using western blotting, protein levels of exosomal tetraspanins were detected. For the in vivo study, Dil-labeled normal and cancer Exos were injected into the tail vein (100 µg exosomal protein/rat) three times at 1-hour intervals. After 24 hours, rats were euthanized and the cellular uptake of Exos was monitored in different organs using immunofluorescence staining (IF). Results: The size distribution and mean zeta potential of HUVEC and MDA-MB-231 cells Exos were 80±29.94 and 64.77±25.49 nm, and -7.58 and -11.8 mV, respectively. Western blotting revealed CD9, CD81, and CD63 in normal and cancer Exos. The SEM images exhibited typical nano-sized round-shape Exo particles. IF staining indicated sequestration of administrated Exos in splenic tissue and lungs. The distribution of Exo in kidneys, aorta, and hepatic tissue was less. These features were more evident in the group that received cancer Exos. We found no obvious adverse effects in rats that received normal or cancer Exos. Conclusion: Normal and cancerous xenogeneic human Exos can be sequestrated prominently in splenic tissue and lungs. Novel delivery approaches and engineering tools are helpful in the target delivery of administrated Exos to the injured sites.

Docosahexaenoic Acid Reduced Vascular Endothelial Cell Injury in Diabetic Rats Via the Modulation of Autophagy.

Purpose: Among varied ω-3 polyunsaturated fatty acid types, the therapeutic properties of docosahexaenoic acid (DHA) have been indicated under diabetic conditions in different cell lineages. Here, we investigated the anti-diabetic properties of DHA in rats with type 2 diabetes mellitus (D2M) focusing on autophagy-controlling factors. Methods: D2M was induced in male Wistar rats using a single dose of streptozocin (STZ) and a high-fat diet for 8 weeks. On week 2, diabetic rats received DHA 950 mg/kg/d until the end of the study. After that, rats were euthanized, and aortic and cardiac tissue samples were stained with H&E staining for histological assessment. The expression of adhesion molecules, ICAM-1 and VCAM-1, was measured in heart samples using real-time PCR analysis. Using western blotting, protein levels of BCLN1, LC3, and P62 were measured in D2M rats pre- and post-DHA treatment. Results: Data showed intracellular lipid vacuoles inside the vascular cells, and cardiomyocytes, after induction of D2M and DHA reduced intracellular lipid droplets and in situ inflammatory response. DHA can diminish increased levels of ICAM-1 in diabetic conditions (P Control vs. D2M rats=0.005) and reach near-to-control values (P Control vs. D2M rats=0.28; P D2M rats vs. D2M rats+DHA=0.033). Based on western blotting, D2M slightly increased the BCLN1 and LC3-II/I ratio without affecting P62. DHA promoted the LC3II/I ratio (P=0.303) and reduced P62 (P Control vs. D2M rats+DHA =0.0433; P D2M vs. D2M rats+DHA=0.096), leading to the completion of autophagy flux under diabetic conditions. Conclusion: DHA can reduce lipotoxicity of cardiovascular cells possibly via the activation of adaptive autophagy response in D2D rats.

Electrospun polyhedral oligomeric silsequioxane-poly(carbonate-urea) urethane for fabrication of hemocompatible small-diameter vascular grafts with angiogenesis capacity.

The clinical utility of small-diameter vascular grafts (SDVGs) is limited due to the possibility of thrombosis and intimal hyperplasia. These features can delay the development of a functional endothelial cell (EC) monolayer on the luminal surface of grafts. Therefore, the development and fabrication of vascular grafts (VGs) with comparable extracellular matrix (ECM) functions are mandatory to elicit hemocompatible confluent EC monolayers, and angiogenesis behavior inside the body. To promote the interactions between ECs and the surface of electrospun polyacrylic acid-grafted polyhedral oligomeric silsesquioxane-poly(carbonate-urea)-urethane (PAAc-POSS-PCUU), in this research, the surface of nanofibers was modified by covalently immobilizing extracted soluble proteins from aorta (ESPA) using EDC/NHS chemistry. The ATR-FTIR spectroscopy, WCA, and SEM microscopy confirmed the binding of acrylic acid and soluble vascular proteins on the surface of electrospun fibers. The PAAc-POSS-PCUU nanofibers and engineered biomimetic Pro-PAAc-POSS-PCUU nanofibers exhibited excellent biocompatibility indicated by increased survival rate (p < 0.05). Western blotting revealed the increase of VE-cadherin, Tie-2, vWF, and VEGFR-2 in HUVECs after being plated on PAAc-POSS-PCUU and Pro-PAAc-POSS-PCUU scaffolds, indicating appropriate angiogenesis behavior (p < 0.05). Besides, the antioxidant capacity was induced by the increase of SOD and GPx activity (p < 0.05). Additionally, blood compatibility tests revealed that Pro-PAAc-POSS-PCUU nanofibers accelerate the formation of a single EC layer without hemolysis and platelet adhesion. Taken together, Pro-PAAc-POSS-PCUU nanofibers exhibited excellent blood compatibility, and angiogenesis behavior, making them a promising candidate for clinical applications.

Autophagy modulation effect on homotypic transfer of intracellular components via tunneling nanotubes in mesenchymal stem cells.

BACKGROUND: Recent studies have proved the role of autophagy in mesenchymal stem cell (MSCs) function and regenerative properties. How and by which mechanism autophagy modulation can affect the juxtacrine interaction of MSCs should be addressed. Here, the role of autophagy was investigated in the formation of tunneling nanotubes (TNTs) and homotypic mitochondrial donation. METHODS: MSCs were incubated with 15 µM Metformin (Met) and/or 3 µM 3-methyladenine (3-MA) for 48 h. The formation of TNTs was assessed using bright-field and SEM images. The mitochondria density and ΔΨ values were monitored using flow cytometry analysis. Using RT-PCR and protein array, the close interaction and shared mediators between autophagy, apoptosis, and Wnt signaling pathways were also monitored. The total fatty acid profile was assessed using gas chromatography. RESULT: Data indicated the increase of TNT length and number, along with other cell projections after the induction of autophagy while these features were blunted in 3-MA-treated MSCs (p < 0.05). Western blotting revealed the significant reduction of Rab8 and p-FAK in 3-MA-treated MSCs (p < 0.05), indicating the inhibition of TNT assembly and vesicle transport. Likewise, the stimulation of autophagy increased autophagic flux and mitochondrial membrane integrity compared to 3-MA-treated MSCs. Despite these findings, protein levels of mitochondrial membrane Miro1 and 2 were unchanged after autophagy inhibition/stimulation (p > 0.05). We found that the inhibition/stimulation of autophagy can affect the protein, and transcription levels of several mediators related to Wnt and apoptosis signaling pathways involved in different cell bioactivities. Data confirmed the profound increase of mono and polyunsaturated/saturated fatty acid ratio in MSCs exposed to autophagy stimulator. CONCLUSIONS: In summary, autophagy modulation could affect TNT formation which is required for homotypic mitochondrial donation. Thus, the modulation of autophagy creates a promising perspective to increase the efficiency of cell-based therapies.

Endothelial progenitor cells for fabrication of engineered vascular units and angiogenesis induction.

The promotion of vascularization and angiogenesis in the grafts is a crucial phenomenon in the healing process and tissue engineering. It has been shown that stem cells, especially endothelial progenitor cells (EPCs), can stimulate blood vessel formation inside the engineered hydrogels after being transplanted into the target sites. The incorporation of EPCs into the hydrogel can last the retention time, long-term survival, on-target delivery effects, migration and differentiation into mature endothelial cells. Despite these advantages, further modifications are mandatory to increase the dynamic growth and angiogenesis potential of EPCs in in vitro and in vivo conditions. Chemical modifications of distinct composites with distinct physical properties can yield better regenerative potential and angiogenesis during several pathologies. Here, we aimed to collect recent findings related to the application of EPCs in engineered vascular grafts and/or hydrogels for improving vascularization in the grafts. Data from the present article can help us in the application of EPCs as valid cell sources in the tissue engineering of several ischemic tissues.

Toxoplasma gondii suppress human cord blood cell differentiation to the NK cell population.

BACKGROUND: Toxoplasma gondii is an obligate intracellular protozoan parasite that can invade all mammalian cells. It is well established that natural killer (NK) cells have critical protective roles in innate immunity during infections by intracellular pathogens. In the current study, we conducted an in vitro experiment to evaluate NK cell differentiation and activation from human umbilical cord blood mononuclear cells (UCB-MNCs) after infection with T. gondii tachyzoites. METHODS: UCB-MNCs were infected by fresh tachyzoites of type I (RH) or type II (PTG) strains of T. gondii pre-expanded in mesenchymal stem cells for 2 weeks in a medium enriched with stem cell factor, Flt3, IL-2, and IL-15. Flow cytometry analysis and western blot analysis were performed to measure the CD57+, CD56+, and Granzyme A (GZMA). RESULTS: Data revealed that incubation of UCB-MNCs with NK cell differentiation medium increased the CD57+, CD56+, and GZMA. UCB-MNCs cocultured with PTG tachyzoites showed a significant reduction of CD56+ and GZMA, but nonsignificant changes, in the levels of CD56+ compared to the control UCB-MNCs (p > .05). Noteworthy, 2-week culture of UCB-MNCs with type I (RH) tachyzoites significantly suppressed CD57+, CD56+, and GZMA, showing reduction of NK cell differentiation from cord blood cells. CONCLUSION: Our findings suggest that virulent T. gondii tachyzoites with cytopathic effects inhibit NK cell activation and eliminate innate immune responses during infection, and consequently enable the parasite to continue its survival in the host body.

Relationship between angiogenesis biomarker endocan and apolipoproteins in patients with acute myocardial infarction.

Aim: In the current study, serum levels of endocan in patients attended with ST-elevation myocardial infarction, as well as the possible correlation with apolipoprotein-A1 (APO-A1) and APO-B were investigated. Materials & methods: In 80 men, endocan, cTnI, APO-A1, and APO-B levels were measured. Finally, the correlation of endocan with APO-A1, APO-B, and APO-B/ APO-A1 ratio was assessed. Results: Significant changes in APO-A1, APO-B, endocan levels, and APO-B/APO-A1 ratio were found in acute myocardial infarction cases compared with the control arm (p < 0.05). In addition, our finding showed a significant correlation between APO-B and endocan levels, but not APO-A. Conclusion: High endocan level is an independent indicator of endothelial dysfunction and ischemic cardiovascular conditions, which could be related to APO-B.

[Box: see text].

Exosomes as a therapeutic tool to promote neurorestoration and cognitive function in neurological conditions: Achieve two ends with a single effort.

Exosomes possess a significant role in intercellular communications. In the nervous system, various neural cells release exosomes that not only own a role in intercellular communications but also eliminate the waste of cells, maintain the myelin sheath, facilitate neurogenesis, and specifically assist in normal cognitive function. In neurological conditions including Parkinson's disease (PD), Alzheimer's disease (AD), traumatic brain injury (TBI), and stroke, exosomal cargo like miRNAs take part in the sequela of conditions and serve as a diagnostic tool of neurological disorders, too. Exosomes are not only a diagnostic tool but also their inhibition or administration from various sources like mesenchymal stem cells and serum, which have shown a worthy potential to treat multiple neurological disorders. In addition to neurodegenerative manifestations, cognitive deficiencies are an integral part of neurological diseases, and applying exosomes in improving both aspects of these diseases has been promising. This review discusses the status of exosome therapy in improving neurorestorative and cognitive function following neurological disease.

Mesenchymal stem cell-derived exosomes improve neurogenesis and cognitive function of mice with methamphetamine addiction: A novel treatment approach.

BACKGROUND: Methamphetamine (METH) is a psychostimulant substance with highly addictive and neurotoxic effects, but no ideal treatment option exists to improve METH-induced neurocognitive deficits. Recently, mesenchymal stem cells (MSCs)-derived exosomes have raised many hopes for treating neurodegenerative sequela of brain disorders. This study aimed to determine the therapeutic potential of MSCs-derived exosomes on cognitive function and neurogenesis of METH-addicted rodents. METHODS: Male BALB/c mice were subjected to chronic METH addiction, followed by intravenous administration of bone marrow MSCs-derived exosomes. Then, the spatial memory and recognition memory of animals were assessed by the Barnes maze and the novel object recognition test (NORT). The neurogenesis-related factors, including NeuN and DCX, and the expression of Iba-1, a microglial activation marker, were assessed in the hippocampus by immunofluorescence staining. Also, the expression of inflammatory cytokines, including TNF-α and NF-κB, were evaluated by western blotting. RESULTS: The results showed that BMSCs-exosomes improved the time spent in the target quadrant and correct-to-wrong relative time in the Barnes maze. Also, NORT's discrimination index (DI) and recognition index (RI) were improved following exosome therapy. Additionally, exosome therapy significantly increased the expression of NeuN and DCX in the hippocampus while decreasing the expression of inflammatory cytokines, including TNF-α and NF-κB. Besides, BMSC-exosomes down-regulated the expression of Iba-1. CONCLUSION: Our findings indicate that BMSC-exosomes mitigated METH-caused cognitive dysfunction by improving neurogenesis and inhibiting neuroinflammation in the hippocampus.

Multiprotein collagen/keratin hydrogel promoted myogenesis and angiogenesis of injured skeletal muscles in a mouse model.

Volumetric loss is one of the challenging issues in muscle tissue structure that causes functio laesa. Tissue engineering of muscle tissue using suitable hydrogels is an alternative to restoring the physiological properties of the injured area. Here, myogenic properties of type I collagen (0.5%) and keratin (0.5%) were investigated in a mouse model of biceps femoris injury. Using FTIR, gelation time, and rheological analysis, the physicochemical properties of the collagen (Col)/Keratin scaffold were analyzed. Mouse C2C12 myoblast-laden Col/Keratin hydrogels were injected into the injury site and histological examination plus western blotting were performed to measure myogenic potential after 15 days. FTIR indicated an appropriate interaction between keratin and collagen. The blend of Col/Keratin delayed gelation time when compared to the collagen alone group. Rheological analysis revealed decreased stiffening in blended Col/Keratin hydrogel which is favorable for the extrudability of the hydrogel. Transplantation of C2C12 myoblast-laden Col/Keratin hydrogel to injured muscle tissues led to the formation of newly generated myofibers compared to cell-free hydrogel and collagen groups (p < 0.05). In the C2C12 myoblast-laden Col/Keratin group, a low number of CD31+ cells with minimum inflammatory cells was evident. Western blotting indicated the promotion of MyoD in mice that received cell-laden Col/Keratin hydrogel compared to the other groups (p < 0.05). Despite the increase of the myosin cell-laden Col/Keratin hydrogel group, no significant differences were obtained related to other groups (p > 0.05). The blend of Col/Keratin loaded with myoblasts provides a suitable myogenic platform for the alleviation of injured muscle tissue.

Exosomes encapsulated in hydrogels for effective central nervous system drug delivery.

The targeted delivery of pharmacologically active molecules, metabolites, and growth factors to the brain parenchyma has become one of the major challenges following the onset of neurodegeneration and pathological conditions. The therapeutic effect of active biomolecules is significantly impaired after systemic administration in the central nervous system (CNS) because of the blood-brain barrier (BBB). Therefore, the development of novel therapeutic approaches capable of overcoming these limitations is under discussion. Exosomes (Exo) are nano-sized vesicles of endosomal origin that have a high distribution rate in biofluids. Recent advances have introduced Exo as naturally suitable bio-shuttles for the delivery of neurotrophic factors to the brain parenchyma. In recent years, many researchers have attempted to regulate the delivery of Exo to target sites while reducing their removal from circulation. The encapsulation of Exo in natural and synthetic hydrogels offers a valuable strategy to address the limitations of Exo, maintaining their integrity and controlling their release at a desired site. Herein, we highlight the current and novel approaches related to the application of hydrogels for the encapsulation of Exo in the field of CNS tissue engineering.

Tumoricidal properties of thymoquinone on human colorectal adenocarcinoma cells via the modulation of autophagy.

Colorectal cancer (CRC) is deadly anaplastic changes in the gastrointestinal tract with high-rate mortality. In recent years, the application of phytocompounds has been extended along with different therapeutic protocols. Here, we monitored the effects of Thymoquinone (TQ) on autophagy via mitochondrial function after modulation of the Wnt/ß-catenin signaling pathway.Human colorectal adenocarcinoma HT-29 cells were treated with TQ (60 µM) and 15 µM Wnt3a inhibitor (LGK974) for 48 h. The survival rate was evaluated using an MTT assay. The expression of Wnt-related factors (c-Myc, and Axin), angiogenesis (VE-Cadherin), and mitophagy-related factors (PINK1, OPTN) was assessed using real-time PCR assay. Protein levels of autophagy factors (Beclin-1, LC3, and P62) were monitored using western blotting. Using flow cytometry analysis, the intracellular accumulation of Rhodamine 123 was evaluated. The migration properties were analyzed using a scratch wound healing assay.Data indicated that TQ can reduce the viability of HT-29 cells compared to the control cells (p < 0.05). The expression of VE-Cadherin was inhibited while the expression of PINK1 was induced in treated cells (p < 0.05). Both LGK974 and TQ-treated cells exhibited activation of autophagy flux (Beclin-1↑, LC3II/I↑, and p62↓) compared to the control group (p < 0.05). TQ can increase intracellular accumulation of Rhodamine 123, indicating the inhibition of efflux mechanisms in cancer cells. Along with these changes, the migration of cells was also reduced (p < 0.05).TQ is a potential phytocompound to alter the dynamic growth of human colorectal HT-29 cells via the modulation of autophagy, and mitophagy-related mechanisms.

Biosensors; a novel concept in real-time detection of autophagy.

Autophagy is an early-stage response with self-degradation properties against several insulting conditions. To date, the critical role of autophagy has been well-documented in physiological and pathological conditions. This process involves various signaling and functional biomolecules, which are involved in different steps of the autophagic response. During recent decades, a range of biochemical analyses, chemical assays, and varied imaging techniques have been used for monitoring this pathway. Due to the complexity and dynamic aspects of autophagy, the application of the conventional methodology for following autophagic progression is frequently associated with a mistake in discrimination between a complete and incomplete autophagic response. Biosensors provide a de novo platform for precise and accurate analysis of target molecules in different biological settings. It has been suggested that these devices are applicable for real-time monitoring and highly sensitive detection of autophagy effectors. In this review article, we focus on cutting-edge biosensing technologies associated with autophagy detection.

Tumorigenic and tumoricidal properties of exosomes in cancers; a forward look.

In recent decades, emerging data have highlighted the critical role of extracellular vesicles (EVs), especially (exosomes) Exos, in the progression and development of several cancer types. These nano-sized vesicles are released by different cell lineages within the cancer niche and maintain a suitable platform for the interchange of various signaling molecules in a paracrine manner. Based on several studies, Exos can transfer oncogenic factors to other cells, and alter the activity of immune cells, and tumor microenvironment, leading to the expansion of tumor cells and metastasis to the remote sites. It has been indicated that the cell-to-cell crosstalk is so complicated and a wide array of factors are involved in this process. How and by which mechanisms Exos can regulate the behavior of tumor cells and non-cancer cells is at the center of debate. Here, we scrutinize the molecular mechanisms involved in the oncogenic behavior of Exos released by different cell lineages of tumor parenchyma. Besides, tumoricidal properties of Exos from various stem cell (SC) types are discussed in detail.

Role of autophagy in angiogenic potential of vascular pericytes.

The vasculature system is composed of a multiplicity of juxtaposed cells to generate a functional biological barrier between the blood and tissues. On the luminal surface of blood vessels, endothelial cells (ECs) are in close contact with circulating cells while supporting basal lamina and pericytes wrap the abluminal surface. Thus, the reciprocal interaction of pericytes with ECs is a vital element in the physiological activity of the vascular system. Several reports have indicated that the occurrence of pericyte dysfunction under ischemic and degenerative conditions results in varied micro and macro-vascular complications. Emerging evidence points to the fact that autophagy, a conserved self-digestive cell machinery, can regulate the activity of several cells like pericytes in response to various stresses and pathological conditions. Here, we aim to highlight the role of autophagic response in pericyte activity and angiogenesis potential following different pathological conditions.