Neuronal activity-induced, equilibrative nucleoside transporter-dependent, somatodendritic adenosine release revealed by a GRAB sensor.

The purinergic signaling molecule adenosine (Ado) modulates many physiological and pathological functions in the brain. However, the exact source of extracellular Ado remains controversial. Here, utilizing a newly optimized genetically encoded GPCR-Activation-Based Ado fluorescent sensor (GRABAdo), we discovered that the neuronal activity-induced extracellular Ado elevation is due to direct Ado release from somatodendritic compartments of neurons, rather than from the axonal terminals, in the hippocampus. Pharmacological and genetic manipulations reveal that the Ado release depends on equilibrative nucleoside transporters but not the conventional vesicular release mechanisms. Compared with the fast-vesicular glutamate release, the Ado release is slow (~40 s) and requires calcium influx through L-type calcium channels. Thus, this study reveals an activity-dependent second-to-minute local Ado release from the somatodendritic compartments of neurons, potentially serving modulatory functions as a retrograde signal.

A novel mechanism of ferroptosis inhibition-enhanced atherosclerotic plaque stability: YAP1 suppresses vascular smooth muscle cell ferroptosis through GLS1.

Atherosclerosis is a leading cause of cardiovascular diseases (CVDs), often resulting in major adverse cardiovascular events (MACEs), such as myocardial infarction and stroke due to the rupture or erosion of vulnerable plaques. Ferroptosis, an iron-dependent form of cell death, has been implicated in the development of atherosclerosis. Despite its involvement in CVDs, the specific role of ferroptosis in atherosclerotic plaque stability remains unclear. In this study, we confirmed the presence of ferroptosis in unstable atherosclerotic plaques and demonstrated that the ferroptosis inhibitor ferrostatin-1 (Fer-1) stabilizes atherosclerotic plaques in apolipoprotein E knockout (Apoe-/-) mice. Using bioinformatic analysis combining RNA sequencing (RNA-seq) with single-cell RNA sequencing (scRNA-seq), we identified Yes-associated protein 1 (YAP1) as a potential key regulator of ferroptosis in vascular smooth muscle cells (VSMCs) of unstable plaques. In vitro, we found that YAP1 protects against oxidized low-density lipoprotein (oxLDL)-induced ferroptosis in VSMCs. Mechanistically, YAP1 exerts its anti-ferroptosis effects by regulating the expression of glutaminase 1 (GLS1) to promote the synthesis of glutamate (Glu) and glutathione (GSH). These findings establish a novel mechanism where the inhibition of ferroptosis promotes the stabilization of atherosclerotic plaques through the YAP1/GLS1 axis, attenuating VSMC ferroptosis. Thus, targeting the YAP1/GLS1 axis to suppress VSMC ferroptosis may represent a novel strategy for preventing and treating unstable atherosclerotic plaques.

Tuning Surface Electronics State of P-Doped In2.77S4/In(OH)3 toward Efficient Photoelectrochemical Water Oxidation.

Indium sulfide with a two-dimensional layered structure offers a platform for catalyzing water oxidation by a photoelectrochemical process. However, the limited hole holders hinder the weak intrinsic catalytic activity. Here, the nonmetallic phosphorus atom is coordinated to In2.77S4/In(OH)3 through a bridge-bonded sulfur atom. By substituting the S position by the P dopant, the work function (surface potential) is regulated from 445 to 210 mV, and the lower surface potential is shown to be beneficial for holding the photogenerated holes. In2.77S4/In(OH)3/P introduces a built-in electric field under the difference of Fermi energy, and the direction is from the bulk to the surface. This band structure results in upward band bending at the interface of In2.77S4/In(OH)3 and P-doped sites, which is identified by density functional theory calculations (∼0.8 eV work function difference). In2.77S4/In(OH)3/P stands out with the highest oxidation efficiency (ηoxi = 70%) and charge separation efficiency (ηsep = 69%). Importantly, it delivers a remarkable water oxidation photocurrent density of 2.51 mA cm-2 under one sun of illumination.

TM6SF2 reduces lipid accumulation in vascular smooth muscle cells by inhibiting LOX-1 and CD36 expression.

TM6SF2, predominantly expressed in the liver and intestine, is closely associated with lipid metabolism. We have demonstrated the presence of TM6SF2 in VSMCs within human atherosclerotic plaques. Subsequent functional studies were conducted to investigate its role in lipid uptake and accumulation in human vascular smooth muscle cells (HAVSMCs) using siRNA knockdown and overexpression techniques. Our results showed that TM6SF2 reduced lipid accumulation in oxLDL-stimulated VSMCs, likely through the regulation of lectin-like oxLDL receptor 1 (LOX-1) and scavenger receptor cluster of differentiation 36 (CD36) expression. We concluded that TM6SF2 plays a role in HAVSMC lipid metabolism with opposing effects on cellular lipid droplet content by downregulation of LOX-1 and CD36 expression.

Integrated multi-omics approach revealed cellular senescence landscape.

Cellular senescence is a complex multifactorial biological phenomenon that plays essential roles in aging, and aging-related diseases. During this process, the senescent cells undergo gene expression altering and chromatin structure remodeling. However, studies on the epigenetic landscape of senescence using integrated multi-omics approaches are limited. In this research, we performed ATAC-seq, RNA-seq and ChIP-seq on different senescent types to reveal the landscape of senescence and identify the prime regulatory elements. We also obtained 34 key genes and deduced that NAT1, PBX1 and RRM2, which interacted with each other, could be the potential markers of aging and aging-related diseases. In summary, our work provides the landscape to study accessibility dynamics and transcriptional regulations in cellular senescence. The application of this technique in different types of senescence allows us to identify the regulatory elements responsible for the substantial regulation of transcription, providing the insights into molecular mechanisms of senescence.

Roles of red mud in remediation of contaminated soil in mining areas: Mechanisms, advances and perspectives.

Red mud (RM) is a kind of strong alkaline solid waste produced from the aluminum industry, which contributes significantly to environmental pollution and can cause severe health issues.Currently, RM is widely recognized as a potential material for soil remediation because of its rich metal oxide content, such as Fe/Al oxides. However, there is no comprehensive description on the roles of RM in passivation remediation of contaminated soil in mining areas. This review summarizes the mechanisms of passivation of heavy metals (HMs) in contaminated soil by RM, including precipitation, adsorption and ion exchange. Besides the effects of adding RM on soil physicochemical properties, heavy metal forms and ecological environment are further elaborated. Moreover, using the co-hydrothermal carbonization of RM and biomass for enhancing the efficiency of contaminated soil remediation is proposed as the main prospective research. This paper provides technical references for the resource utilization of RM and the treatment of heavy metal-contaminated soil.

Self-powered Pt/a-Ga2O3/ITO vertical Schottky junction solar-blind photodetector with excellent detection performance.

Self-powered solar-blind photodetectors (PDs) are promising for military and civilian applications owing to convenient operation, easy preparation, and weak-light sensitivity. In the present study, the solar-blind deep-ultraviolet (DUV) photodetector based on amorphous Ga2O3 (a-Ga2O3) and with a simple vertical stack structure is proposed by applying the low-cost magnetron sputtering technology. By tuning the thickness of the amorphous Ga2O3 layer, the device exhibits excellent detection performance. Under 3 V reverse bias, the photodetector achieves a high responsivity of 671A/W, a high detectivity of 2.21 × 1015 Jones, and a fast response time of 27/11 ms. More extraordinary, with the help of the built-in electric field at the interface, the device achieves an excellent performance in detection when self-powered, with an ultrahigh responsivity of 3.69 A/W and a fast response time of 2.6/6.6 ms under 254 nm light illumination. These results demonstrate its superior performance to most of the self-powered Schottky junction UV photodetectors reported to date. Finally, the Pt/a-Ga2O3/ITO Schottky junction photodiode detector is verified as a good performer in imaging, indicating its applicability in such fields as artificial intelligence, machine vision, and solar-blind imaging.

PCSK9 (Proprotein Convertase Subtilisin/Kexin Type 9) Triggers Vascular Smooth Muscle Cell Senescence and Apoptosis: Implication of Its Direct Role in Degenerative Vascular Disease.

OBJECTIVE: PCSK9 (proprotein convertase subtilisin/kexin type 9) plays a critical role in cholesterol metabolism via the PCSK9-LDLR (low-density lipoprotein receptor) axis in the liver; however, evidence indicates that PCSK9 directly contributes to the pathogenesis of various diseases through mechanisms independent of its LDL-cholesterol regulation. The objective of this study was to determine how PCSK9 directly acts on vascular smooth muscle cells (SMCs), contributing to degenerative vascular disease. Approach and Results: We first examined the effects of PCSK9 on cultured human aortic SMCs. Overexpression of PCSK9 downregulated the expression of ApoER2 (apolipoprotein E receptor 2), a known target of PCSK9. Treatment with soluble recombinant human ApoER2 or the DNA synthesis inhibitor, hydroxyurea, inhibited PCSK9-induced polyploidization and other cellular responses of human SMCs. Treatment with antibodies against ApoER2 resulted in similar effects to those observed with PCSK9 overexpression. Inducible, SMC-specific knockout of Pcsk9 accelerated neointima formation in mouse carotid arteries and reduced age-related arterial stiffness. PCSK9 was expressed in SMCs of human atherosclerotic lesions and abundant in the "shoulder" regions of vulnerable atherosclerotic plaques. PCSK9 was also expressed in SMCs of abdominal aortic aneurysm, which was inversely related to the expression of smooth muscle α-actin. CONCLUSIONS: Our findings demonstrate that PCSK9 inhibits proliferation and induces polyploidization, senescence, and apoptosis, which may be relevant to various degenerative vascular diseases.

Isolation and biological activity of natural chalcones based on antibacterial mechanism classification.

Bacterial infection, which is still one of the leading causes of death in humans, poses an enormous threat to the worldwide public health system. Antibiotics are the primary medications used to treat bacterial diseases. Currently, the discovery of antibiotics has reached an impasse, and due to the abuse of antibiotics resulting in bacterial antibiotic resistance, researchers have a critical desire to develop new antibacterial agents in order to combat the deteriorating antibacterial situation. Natural chalcones, the flavonoids consisting of two phenolic rings and a three-carbon α, ß-unsaturated carbonyl system, possess a variety of biological and pharmacological properties, including anti-cancer, anti-inflammatory, antibacterial, and so on. Due to their potent antibacterial properties, natural chalcones possess the potential to become a new treatment for infectious diseases that circumvents existing antibiotic resistance. Currently, the majority of research on natural chalcones focuses on their synthesis, biological and pharmacological activities, etc. A few studies have been conducted on their antibacterial activity and mechanism. Therefore, this review focuses on the antibacterial activity and mechanisms of seventeen natural chalcones. Firstly, seventeen natural chalcones have been classified based on differences in antibacterial mechanisms. Secondly, a summary of the isolation and biological activity of seventeen natural chalcones was provided, with a focus on their antibacterial activity. Thirdly, the antibacterial mechanisms of natural chalcones were summarized, including those that act on bacterial cell membranes, biological macromolecules, biofilms, and quorum sensing systems. This review aims to lay the groundwork for the discovery of novel antibacterial agents based on chalcones.

IL-17A promotes the progression of Alzheimer's disease in APP/PS1 mice.

BACKGROUND: Alzheimer's disease (AD), which is the most common cause of dementia in elderly individuals, is a progressive neurodegenerative disorder. Neuroinflammation, which is an immune response that is activated by glial cells in the central nervous system, plays an important role in neurodegenerative diseases. Many studies have shown that interleukin-17A (IL-17A) plays an important role in AD, but research on the pathological effects of IL-17A on AD is limited. METHODS: We report the effect of IL-17A on AD progression in APPswe/PS1dE9 (APP/PS1) mice, which are the most widely used AD model mice. The BV2 cell line, which is a microglial cell line derived from C57/BL6 mice, was used to establish a cell model to verify the role of IL-17A in neuroinflammation at the cellular level. The HT22 hippocampal neuronal cell line was used to investigate the relationship between IL-17A and Aß deposition. RESULTS: In this research, we found that IL-17A promotes the progression of AD in the APP/PS1 mouse model. The role of IL-17A in neuroinflammation is related to tumour necrosis factor (TNF)-α. Circulating IL-17A stimulates the secretion of TNF-α by microglia through the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signalling pathway, thus exacerbating neuroinflammation. In addition, intraperitoneal injection of IL-17A antibody (IL17Ab) significantly improved the cognitive function of APP/PS1 mice. CONCLUSIONS: IL-17A increased TNF-α levels in the brain and exacerbated neuroinflammation through the TLR4/NF-κB signalling pathway and microglial activation in APP/PS1 mice. Moreover, IL-17A promoted the progression of AD by enhancing neuroinflammation, inhibiting microglial phagocytosis, and promoting the deposition of ß-amyloid 42 in AD model mice.

Sunitinib-based Proteolysis Targeting Chimeras (PROTACs) reduced the protein levels of FLT-3 and c-KIT in leukemia cell lines.

Proteolysis Targeting Chimeras (PROTACs) based on multi-target inhibitors have been reported several times recently. The advantages of PROTACs technology and the synergistic mechanism of multi-target drugs endow this class of protein degraders with special research significance. Herein, twelve new PROTACs based on Sunitinib and VHL-ligand were synthesized and evaluated for their in vitro anticancer activities. Among them, PROTACs 5 (IC50 = 2.9 ± 1.5 µM) exhibited the most significant antiproliferative activity against HL-60 cells. Western blot results showed that PROTAC 5 reduced the protein levels of FLT-3 and c-KIT in HL-60 cells, and induced the degradation of FLT-3 via the ubiquitin-proteasome system. Moreover, PROTACs 5 and 6 reduced the protein levels of FLT-3 in K562 cells. These results suggest that PROTAC 5 has the potential for further research, especially in combination with small molecule kinase inhibitors to study multidrug resistance of tyrosine kinase inhibitors in cancer treatment.

The position of financial prudence, social influence, and environmental satisfaction in the sustainable consumption behavioural model: Cross-market intergenerational investigation during the Covid-19 pandemic.

The main purpose of this study is to gain an in-depth understanding of the impact of financial prudence (FIN) on social influence and environmental satisfaction in the sustainable consumption (SC) behavioural model from a cross-market intergenerational perspective in the context of COVID-19. Surprisingly, we discovered that, during the COVID-19 pandemic, significant differences emerge between the Chinese and European markets in the four factors (social influence, SC behaviour, environmental satisfaction, and FIN). Unpredictably, Generation X in the European market and Generation Y in the Chinese market had the highest FIN during the pandemic. Another substantial contribution is that, during the epidemic, the influence of social interaction promotes SC behaviour and social influence motivates users to implement SC behaviours by enhancing environmental satisfaction. However, differences arise in the moderating effect of FIN. In China, the moderating effect occurs in the relationship between social influence and SC behaviour, whereas, in Europe, it reflects in the relationship between social influence and environmental satisfaction.

Recent progress in the use of mitochondrial membrane permeability transition pore in mitochondrial dysfunction-related disease therapies.

Mitochondria have various cellular functions, including ATP synthesis, calcium homeostasis, cell senescence, and death. Mitochondrial dysfunction has been identified in a variety of disorders correlated with human health. Among the many underlying mechanisms of mitochondrial dysfunction, the opening up of the mitochondrial permeability transition pore (mPTP) is one that has drawn increasing interest in recent years. It plays an important role in apoptosis and necrosis; however, the molecular structure and function of the mPTP have still not been fully elucidated. In recent years, the abnormal opening up of the mPTP has been implicated in the development and pathogenesis of diverse diseases including ischemia/reperfusion injury (IRI), neurodegenerative disorders, tumors, and chronic obstructive pulmonary disease (COPD). This review provides a systematic introduction to the possible molecular makeup of the mPTP and summarizes the mitochondrial dysfunction-correlated diseases and highlights possible underlying mechanisms. Since the mPTP is an important target in mitochondrial dysfunction, this review also summarizes potential treatments, which may be used to inhibit pore opening up via the molecules composing mPTP complexes, thus suppressing the progression of mitochondrial dysfunction-related diseases.

Cu3P-Ni2P Hybrid Hexagonal Nanosheet Arrays for Efficient Hydrogen Evolution Reaction in Alkaline Solution.

The development of efficient and low-cost hydrogen evolution reaction electrocatalysts has been regarded as a promising approach to produce sustainable and clean fuels to solve the energy crisis and environmental problems. Herein, 3D hybrid Cu3P-Ni2P hexagonal nanosheet arrays are successfully prepared on nickel foam (Cu3P-Ni2P/NF). Benefiting from synergistic effects and strong chemical coupling existing at the interface, the Cu3P-Ni2P/NF electrode exhibits a low overpotential of 103 mV at a current density of 10 mA cm-2, which is 47 and 100 mV less than that for Ni2P/NF and Cu3P/NF, respectively. It also shows excellent electrochemical durability for long-term reaction in alkaline medium. The excellent electrocatalytic activity makes the Cu3P-Ni2P/NF as a promising cathode toward efficient hydrogen evolution via electrochemical water splitting.

iPSC-derived mesenchymal stem cells exert SCF-dependent recovery of cigarette smoke-induced apoptosis/proliferation imbalance in airway cells.

Mesenchymal stem cells (MSCs) have emerged as a potential cell-based therapy for pulmonary emphysema in animal models. Our previous study demonstrated that human induced pluripotent stem cell-derived MSCs (iPSC-MSCs) were superior over bone marrow-derived MSCs (BM-MSCs) in attenuating cigarette smoke (CS)-induced airspace enlargement possibly through mitochondrial transfer. This study further investigated the effects of iPSC-MSCs on inflammation, apoptosis, and proliferation in a CS-exposed rat model and examined the effects of the secreted paracrine factor from MSCs as another possible mechanism in an in vitro model of bronchial epithelial cells. Rats were exposed to 4% CS for 1 hr daily for 56 days. At days 29 and 43, human iPSC-MSCs or BM-MSCs were administered intravenously. We observed significant attenuation of CS-induced elevation of circulating 8-isoprostane and cytokine-induced neutrophil chemoattractant-1 after iPSC-MSC treatment. In line, a superior capacity of iPSC-MSCs was also observed in ameliorating CS-induced infiltration of macrophages and neutrophils and apoptosis/proliferation imbalance in lung sections over BM-MSCs. In support, the conditioned medium (CdM) from iPSC-MSCs ameliorated CS medium-induced apoptosis/proliferation imbalance of bronchial epithelial cells in vitro. Conditioned medium from iPSC-MSCs contained higher level of stem cell factor (SCF) than that from BM-MSCs. Deprivation of SCF from iPSC-MSC-derived CdM led to a reduction in anti-apoptotic and pro-proliferative capacity. Taken together, our data suggest that iPSC-MSCs may possess anti-apoptotic/pro-proliferative capacity in the in vivo and in vitro models of CS-induced airway cell injury partly through paracrine secretion of SCF.

Preparation of ZnO:Eu3+ nanospheres via a micro-emulsion method and analysis of the photoluminescence properties.

ZnO:Eu3+ nanospheres were prepared via a micro-emulsion method with hexadecyl trimethyl ammonium bromide as the primary surfactant, butanol as the cosurfactant and octane as the oil phase. The X-ray diffraction (XRD) pattern suggests that the Eu3+ ions have entered into the ZnO lattices. Scanning electron microscopy (SEM) images show that large scale-shaped nanospheres about 200-500 nm in size were formed. The photoluminescence (PL) spectra suggest that the Eu3+ ions doped into ZnO have located at the non-inversion center positions because only the 612 nm peak (5D0 --> 7F2) occurred in the emission spectra. A schematic drawing for the possible mechanisms of electron transitions in the PL excitation and emission spectra is also proposed.

Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease.

Amyloid plaques, a major pathological hallmark of Alzheimer's disease (AD), are caused by an imbalance between the amyloidogenic and non-amyloidogenic pathways of amyloid precursor protein (APP). BACE1 cleavage of APP is the rate-limiting step for amyloid-ß production and plaque formation in AD. Although the alteration of BACE1 expression in AD has been investigated, the underlying mechanisms remain unknown. In this study, we determined MEIS2 was notably elevated in AD models and AD patients. Alterations in the expression of MEIS2 can modulate the levels of BACE1. MEIS2 downregulation improved the learning and memory retention of AD mice and decreased the number of amyloid plaques. MEIS2 binds to the BACE1 promoter, positively regulates BACE1 expression, and accelerates APP amyloid degradation in vitro. Therefore, our findings suggest that MEIS2 might be a critical transcription factor in AD, since it regulates BACE1 expression and accelerates BACE1-mediated APP amyloidogenic cleavage. MEIS2 is a promising early intervention target for AD treatment.

Synaptic vesicle glycoprotein 2 A in serum is an ideal biomarker for early diagnosis of Alzheimer's disease.

BACKGROUND: Previous studies have demonstrated that early intervention was the best plan to inhibit the progression of Alzheimer's disease (AD), which relied on the discovery of early diagnostic biomarkers. In this study, synaptic vesicle glycoprotein 2 A (SV2A) was examined to improve the early diagnostic efficiency in AD. METHODS: In this study, biomarker testing was performed through the single-molecule array (Simoa). A total of 121 subjects including cognitively unimpaired controls, amnestic mild cognitive impairment (aMCI), AD and other types of dementia underwent cerebrospinal fluid (CSF) SV2A testing; 430 subjects including health controls, aMCI, AD and other types of dementia underwent serum SV2A, glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL) and p-tau217 testing; 92 subjects including aMCI and AD underwent both CSF SV2A and serum SV2A testing; 115 cognitively unimpaired subjects including APOE ε4 carriers and APOE ε4 non-carriers were tested for serum SV2A, GFAP, NfL and p-tau217. Then, the efficacy of SV2A for the early diagnosis of AD and its ability to identify those at high risk of AD from a cognitively unimpaired population were further analyzed. RESULTS: Both CSF and serum SV2A significantly and positively correlated with cognitive performance in patients with AD, and their levels gradually decreased with the progression of AD. Serum SV2A demonstrated excellent diagnostic efficacy for aMCI, with a sensitivity of 97.8%, which was significantly higher than those of NfL, GFAP, and p-tau217. The SV2A-positive rates ranged from 92.86 to 100% in aMCI cases that were negative for the above three biomarkers. Importantly, of all the biomarkers tested, serum SV2A had the highest positivity rate (81.82%) in individuals at risk for AD. CONCLUSIONS: Serum SV2A was demonstrated to be a novel and ideal biomarker for the early diagnosis of AD, which can effectively distinguish those at high risk of AD in cognitively unimpaired populations.

Novel treatments against airway inflammation in COPD based on drug repurposing.

Chronic obstructive pulmonary disease (COPD) is a major cause of death and reduces quality of life that contributes to a health problem worldwide. Chronic airway inflammation is a hallmark of COPD, which occurs in response to exposure of inhaled irritants like cigarette smoke. Despite accessible to the most up-to-date medications, none of the treatments is currently available to decrease the disease progression. Therefore, it is believed that drugs which can reduce airway inflammation will provide effective disease modifying therapy for COPD. There are many broad-range anti-inflammatory drugs including those that inhibit cell signaling pathways like inhibitors of p38 mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB), and phosphoinositide-3-kinase (PI3K), are now in phase III development for COPD. In this chapter, we review recent basic research data in the laboratory that may indicate novel therapeutic pathways arisen from currently used drugs such as selective monoamine oxidase (MAO)-B inhibitors and drugs targeting peripheral benzodiazepine receptors [also known as translocator protein (TSPO)] to reduce airway inflammation. Considering the impact of chronic airway inflammation on the lives of COPD patients, the potential pharmacological candidates for new anti-inflammatory targets should be further investigated. In addition, it is crucial to consider the phenotypes/molecular endotypes of COPD patients together with specific outcome measures to target novel therapies. This review will enhance our knowledge on how cigarette smoke affects MAO-B activity and TSPO activation/inactivation with specific ligands through regulation of mitochondrial function, and will help to identify new potential treatment for COPD in future.

Long Non-Coding RNAs of Plants in Response to Abiotic Stresses and Their Regulating Roles in Promoting Environmental Adaption.

Abiotic stresses triggered by climate change and human activity cause substantial agricultural and environmental problems which hamper plant growth. Plants have evolved sophisticated mechanisms in response to abiotic stresses, such as stress perception, epigenetic modification, and regulation of transcription and translation. Over the past decade, a large body of literature has revealed the various regulatory roles of long non-coding RNAs (lncRNAs) in the plant response to abiotic stresses and their irreplaceable functions in environmental adaptation. LncRNAs are recognized as a class of ncRNAs that are longer than 200 nucleotides, influencing a variety of biological processes. In this review, we mainly focused on the recent progress of plant lncRNAs, outlining their features, evolution, and functions of plant lncRNAs in response to drought, low or high temperature, salt, and heavy metal stress. The approaches to characterize the function of lncRNAs and the mechanisms of how they regulate plant responses to abiotic stresses were further reviewed. Moreover, we discuss the accumulating discoveries regarding the biological functions of lncRNAs on plant stress memory as well. The present review provides updated information and directions for us to characterize the potential functions of lncRNAs in abiotic stresses in the future.